BEGIN:VCALENDAR VERSION:2.0 PRODID:talks.ox.ac.uk BEGIN:VEVENT SUMMARY:The perineurium integrates leptin with its sympathetic outflow to protect against obesity - Dr Gitalee Sarker (DPAG\, University of Oxford) DTSTART;VALUE=DATE-TIME:20260227T160000Z DTEND;VALUE=DATE-TIME:20260227T170000Z UID:https://talks.ox.ac.uk/talks/id/5a24d278-7397-436a-8fdb-96e043fc17a0/ DESCRIPTION:The regulatory mechanism of leptin's afferent action in the br ain\, constituting a negative feedback loop\, is contingent upon the effer ent sympathetic innervation of white and brown adipose tissues. Nonetheles s\, the peripheral regulation governing the relative strengths of the affe rent and efferent arms remains ambiguous. Using single-cell RNA sequencing on murine sympathetic ganglia\, we identified the enriched expression of both the leptin receptor (Lepr) and the β2 adrenergic receptor (Adrb2) in perineurial cells that form a barrier around sympathetic ganglia and nerv e bundles in adipose tissues. We show that Lepr+ Sympathetic Perineurial C ells (SPCs) are molecularly similar to endothelial cells and that conditio nal knockout of Adrb2 in Lepr+ SPCs predisposes mice to obesity by lowerin g the energy expenditure and thermogenic activity without affecting food i ntake. The obesogenic phenotype was exclusively observed in male mice. Not ably\, we found that hyperleptinemia associated with obesity causes apopto sis in SPCs\, leading to a significant erosion of the perineurial barrier and concomitant adipose sympathetic neuropathy. We further show that this deleterious effect can be reversed by partial reduction of leptin or by sy mpathomimetic β2 adrenergic receptor agonism. These results have relevanc e to human obesity\, as we observed a male-specific synergistic effect of highly common polymorphisms of LEPR and ADRB2 on the risk of increased BMI in a large European population. We propose that SPCs coordinate the affer ent and efferent arms of the neuroendocrine loop of leptin action to regul ate energy expenditure and body weight.\nSpeakers:\nDr Gitalee Sarker (DPA G\, University of Oxford) LOCATION:This is a virtual event\; please contact events@dpag.ox.ac.uk for Teams Link TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/5a24d278-7397-436a-8fdb-96e043fc17a0/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:The perineurium integrates leptin with its sympathetic ou tflow to protect against obesity - Dr Gitalee Sarker (DPAG\, University of Oxford) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:A structure-function neuronal network model of the rat nervous sys tem - Professor Larry Swanson (University of Southern California) DTSTART;VALUE=DATE-TIME:20260305T110000Z DTEND;VALUE=DATE-TIME:20260305T120000Z UID:https://talks.ox.ac.uk/talks/id/3404c345-1011-4d99-bc0d-a3074a4ce488/ DESCRIPTION:\nSpeakers:\nProfessor Larry Swanson (University of Southern C alifornia) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/3404c345-1011-4d99-bc0d-a3074a4ce488/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:A structure-function neuronal network model of the rat ne rvous system - Professor Larry Swanson (University of Southern California) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Computing the location(s) of sound(s) in the visual scene - Profes sor Jennifer Groh (Duke University) DTSTART;VALUE=DATE-TIME:20260306T110000Z DTEND;VALUE=DATE-TIME:20260306T120000Z UID:https://talks.ox.ac.uk/talks/id/3a5841bd-8267-4c16-a663-1317dff8e7c8/ DESCRIPTION:I will discuss two topics concerning visual and auditory spati al coding: 1. Early cross-talk between vision and hearing\, in which eye movement signals trigger eardrum oscillations and create faint saccade-rel ated sounds. 2. A new theory of neural coding\, involving multiplexing of signals via fluctuating activity patterns. Such multiplexing could allow representations to encode more than one simultaneous visual or auditory s timulus. These findings emerged from experimentally testing computationa l models\, highlighting the importance of theory in guiding experimental s cience. \nSelected References:\nLovich\, S. N.\, C. D. King\, D. L. Murph y\, R. Landrum\, C. A. Shera and J. M. Groh (2023). "Parametric informatio n about eye movements is sent to the ears." Proceedings of the national ac ademy of sciences 120(48): p. e2303562120.\n\nGroh\, J. M.\, M. N. Schmehl \, V. C. Caruso and S. T. Tokdar (2024). "Signal switching may enhance pro cessing power of the brain." Trends Cogn Sci 28(7): 600-613.\n\nSPEAKER BI OGRAPHY\n\nJennifer M. Groh is Professor of Psychology & Neuroscience\, Ne urobiology\, Computer Science\, and Biomedical Engineering at Duke Univers ity\, where she is a member of the Center for Cognitive Neuroscience and t he Duke Institute for Brain Sciences. Her research concerns how the brain represents spatial information and performs computations on those represe ntations. Her discoveries have shed light on how the brain transforms aud itory signals to permit communication with visual signals - despite major differences in the neural “language” used by each sense. She is the re cipient of numerous awards including a John Simon Guggenheim fellowship. She has authored many scientific publications as well as a well-regarded b ook for a general audience (Making Space: How the Brain Knows Where Things Are\, Harvard University Press\, 2014) and a related popular Coursera cou rse The Brain and Space. \n\nSpeakers:\nProfessor Jennifer Groh (Duke Uni versity) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/3a5841bd-8267-4c16-a663-1317dff8e7c8/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Computing the location(s) of sound(s) in the visual scene - Professor Jennifer Groh (Duke University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Orexin/hypocretin knockout impairs mouse visual perception\, proce ssing and plasticity\, and disrupts development of the cortical subplate - Dr Cornelia Schöne (University of Göttingen) DTSTART;VALUE=DATE-TIME:20260226T160000Z DTEND;VALUE=DATE-TIME:20260226T170000Z UID:https://talks.ox.ac.uk/talks/id/b43f873b-953d-4146-8605-dcc3cadb8733/ DESCRIPTION:Lateral hypothalamic orexin/hypocretin circuits are required f or stable consciousness: loss of orexin signals causes narcolepsy in human s\, dogs and mice. While orexins activate deep cortical layers in mouse pr imary visual cortex (V1)\, their role for vision remains underexplored. On a behavioral/perceptual level\, orexin knockout (KO) mice had normal visu al acuity\, but worse orientation discrimination\, needing a larger angle difference to discriminate square wave patterns. Using the oddball paradig m\, in which a stimulus is presented frequently (redundant context) or rar ely (oddball context)\, we provide electrophysiological evidence suggestin g disrupted V1 processing of visual signals in anaesthetized orexin KO mic e. This includes delayed peaks of visually evoked potentials (VEP) and dis ruption of context dependent modulation of VEP waveform and power spectra. The cause for these impairments might be developmental in nature: Orexin KO mice showed extended survival of cortical subplate cells and altered de velopment of layer 6 during early postnatal development. As orexins were p reviously shown to specifically activate deep cortical layers\, which driv e high gamma brain states favorable for plasticity\, but that are lost in orexin KO mice\, here we further tested whether orexin KO would impair pla sticity during development. Indeed\, orexin KO disrupted monocular depriva tion induced ocular dominance plasticity specifically during the late crit ical period for visual circuit development\, suggesting disruption of expe rience-dependent plasticity of V1 circuits during this paradigm. Together our data show that loss of orexin peptides affects development of visual c ircuits\, and causes deficits in visual perception\, processing and plasti city.\nSpeakers:\nDr Cornelia Schöne (University of Göttingen) LOCATION:Sherrington Building (Florence Buchanan Lecture Theatre)\, off Pa rks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/b43f873b-953d-4146-8605-dcc3cadb8733/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Orexin/hypocretin knockout impairs mouse visual perceptio n\, processing and plasticity\, and disrupts development of the cortical s ubplate - Dr Cornelia Schöne (University of Göttingen) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Postnatal neuronal migration in health and disease: mechanisms and modulation - Professor Kazunobu Sawamoto (Nagoya City University) DTSTART;VALUE=DATE-TIME:20260129T120000Z DTEND;VALUE=DATE-TIME:20260129T130000Z UID:https://talks.ox.ac.uk/talks/id/96612532-d35b-4395-8ca3-eef3e6c9bd82/ DESCRIPTION:Postnatal neuronal migration contributes to the structural and functional plasticity of the mammalian brain under both physiological and pathological conditions. This talk will focus on the cellular and molecul ar mechanisms that shape migratory modes of immature neurons within comple x tissue environments. I will also discuss how experimental modulation of these mechanisms can be used to dissect migratory principles and to explor e ways to enhance neuronal migration toward functional repair in disease c ontexts.\nSpeakers:\nProfessor Kazunobu Sawamoto (Nagoya City University) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/96612532-d35b-4395-8ca3-eef3e6c9bd82/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Postnatal neuronal migration in health and disease: mecha nisms and modulation - Professor Kazunobu Sawamoto (Nagoya City University ) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Serotonergic modulation of hippocampal-thalamic circuit excitabili ty - Professor Sharon Swanger (Virginia Tech) DTSTART;VALUE=DATE-TIME:20260219T110000Z DTEND;VALUE=DATE-TIME:20260219T120000Z UID:https://talks.ox.ac.uk/talks/id/60dd1867-0cde-4b99-b91f-9a49f9735e9f/ DESCRIPTION:Serotonergic inputs innervate nearly the entire brain and broa dly influence behavior\, but how serotonin shapes neural circuit function at the synaptic and cellular levels remain poorly understood. The Swanger lab has discovered cell-type-specific mechanisms by which serotonin regula tes communication between the hippocampus and anterior nucleus of the thal amus. This seminar will discuss how serotonin influences excitation and i nhibition within this circuitry as well as the lab's ongoing work investig ating how targeting serotonin signaling counteracts circuit hyperexcitabil ity in an epilepsy mouse model.\nSpeakers:\nProfessor Sharon Swanger (Virg inia Tech) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/60dd1867-0cde-4b99-b91f-9a49f9735e9f/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Serotonergic modulation of hippocampal-thalamic circuit e xcitability - Professor Sharon Swanger (Virginia Tech) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Myelin Plasticity: a New Neural Circuit Modifier for Opioid Reward - Dr Belgin Yalçın (Stanford University) DTSTART;VALUE=DATE-TIME:20260121T150000Z DTEND;VALUE=DATE-TIME:20260121T160000Z UID:https://talks.ox.ac.uk/talks/id/e96bc3d3-bfde-4ef2-95aa-938d25eaa683/ DESCRIPTION:Neural activity-regulated myelin plasticity is increasingly re cognized as a dynamic regulator of neural circuit function shaping cogniti on and learning. However\, its role in pathological circuit remodelling re mains largely unexplored. Drugs of abuse\, including opioids such as morph ine\, target the dopaminergic reward system and drive persistent synaptic and circuit-level modifications. Although microglia and astrocytes have be en implicated in these adaptations\, the contribution of myelin-forming ol igodendroglial lineage cells\, which are uniquely positioned to modify cir cuit function\, has remained unknown. In this talk\, I will discuss our fi ndings demonstrating that myelin plasticity is a key modulator of dopamine rgic circuit function and opioid reward. Increased dopaminergic neuron act ivity\, evoked by either optogenetic stimulation or morphine\, induces oli godendrogenesis within the reward system in a circuit- and region-specific manner. Disrupting this myelin plasticity through conditional blockade of oligodendrogenesis abrogates morphine-associated reward learning\, identi fying oligodendroglial cells as critical regulators of reward behaviour. R eal-time dopamine recordings reveal that myelin plasticity is necessary fo r modulating network synchrony and ensuring a timely dopamine release requ ired for reward learning. Our findings establish myelin plasticity as a pr eviously unappreciated feature of dopaminergic reward circuitry that criti cally contributes to the behavioural reinforcing effects of opioids.\nSpea kers:\nDr Belgin Yalçın (Stanford University) LOCATION:This is a virtual event\; please contact events@dpag.ox.ac.uk for Teams Link TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/e96bc3d3-bfde-4ef2-95aa-938d25eaa683/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Myelin Plasticity: a New Neural Circuit Modifier for Opio id Reward - Dr Belgin Yalçın (Stanford University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Endovascular Intra-arterial Delivery of D24-RGD-loaded MSCs for di ffuse midline glioma - Dr Christopher Young (University of Texas) DTSTART;VALUE=DATE-TIME:20251204T113000Z DTEND;VALUE=DATE-TIME:20251204T123000Z UID:https://talks.ox.ac.uk/talks/id/f72b4c65-2b62-4291-ba1d-20002deca5ad/ DESCRIPTION:Introduction:\nDiffuse midline glioma (DMG)/diffuse intrinsic pontine glioma (DIPG) are deadly childhood gliomas with median survival of less than 12 months and a 2 year survival of 10%. D24\, a genetically eng ineered adenovirus specific for glioma\, has anti-tumoral effect in a phas e 1 study when given by direct intratumoral injection. Our preliminary wor k has shown endovascular super-selective intra-arterial delivery of D24 pa ckaged in mesenchymal stem cells (MSC-D24) is feasible and safe in patient s. \nObjective:\nWe hypothesize that endovascular intra-arterial delivery of MSC-D24 will be safe and effective for treatment of DMG/DIPG.\nMethods: \nIn vitro killing assays were used to assess the tumoricidal effects of M SC-D24 against DIPG using TP54\, DIPG 36\, and SF8628 cell lines (from 102 to 105 cells). Transwell migration assays were performed to test homing o f MSC (105 cells) to the same cell lines. To assess safety of infusion in the vertebrobasilar circulation\, a rabbit survival model (7 days) was use d and 0.4 mL of 107 MSC-D24 cells were infused into the basilar artery. Cl inical examination\, histology\, angiography\, and MRI were used to assess stroke and other complications after infusion. The efficacy of MSC-D24 ag ainst will be tested in-vivo using a mice xenograft model of DIPG.\nResult s:\nTranswell killing assays showed a dose dependent tumoricidal effects o f MSC-D24 against all 3 DIPG cell lines. MSCs successfully homed to TP54 i n the migration assay. Rabbits (n=3) did not exhibit neurologic deficits a fter the MSC-D24 intra-arterial infusion and MRI\, histology\, and angiogr aphy post-infusion did not show any strokes or other evidence of tissue in jury. Bioluminescent imaging of DIPG bearing mice showed tumor reduction a nd improved survival.\nConclusion:\nEndovascular vertebrobasilar intra-art erial infusion of MSC-D24 is safe and the oncolytic virus appears effectiv e against DIPG in both in vitro and in vivo models. The results support a phase 1 trial of MSC-D24 for patients with DMG/DIPG.\nSpeakers:\nDr Christ opher Young (University of Texas) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/f72b4c65-2b62-4291-ba1d-20002deca5ad/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Endovascular Intra-arterial Delivery of D24-RGD-loaded MS Cs for diffuse midline glioma - Dr Christopher Young (University of Texas) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Axo-spinous communication between the cortex and thalamus - Profes sor László Acsády (Hungarian Research Network\, Institute of Experiment al Medicine) DTSTART;VALUE=DATE-TIME:20260113T160000Z DTEND;VALUE=DATE-TIME:20260113T170000Z UID:https://talks.ox.ac.uk/talks/id/73ff2701-9c2f-4805-a0cc-afbf69e4856c/ DESCRIPTION:Spines are ubiquitous morpho-functional elements of excitatory synaptic transmission and plasticity in the neocortex. Whether functional spines are also present in the thalamus is currently unclear. Here I demo nstrate that layer 5 cortico-thalamic terminals arising from several front al cortical regions preferentially target functional spines in the thalamu s via variable and complex synapses. These axo-spinous L5-thalamic connect ions are surprisingly powerful\, able to selectively recruit a subset of t halamic neuron and are involved in motor learning. \nSpeakers:\nProfessor László Acsády (Hungarian Research Network\, Institute of Experimental M edicine) LOCATION:Sherrington Building (Florence Buchanan Lecture Theatre)\, off Pa rks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/73ff2701-9c2f-4805-a0cc-afbf69e4856c/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Axo-spinous communication between the cortex and thalamus - Professor László Acsády (Hungarian Research Network\, Institute of E xperimental Medicine) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Cortical alterations in Spinal Muscular Atrophy - Professor Alessa ndro Vercelli (University of Torino) DTSTART;VALUE=DATE-TIME:20251204T120000Z DTEND;VALUE=DATE-TIME:20251204T130000Z UID:https://talks.ox.ac.uk/talks/id/c069ece9-41a1-46ee-b871-da5956ff1bcb/ DESCRIPTION:Spinal Muscular Atrophy (SMA) is a neuromuscular disease due t o the lack of Survival Motor Neuron (SMN) protein\, characterized by lower motor neuron (MN) degeneration and muscle atrophy. However\, evidence sho ws that SMA patients display brain abnormalities correlating with disease severity\, suggesting altered maturation and maladaptive plasticity potent ially contributing to cortical alterations. Our previous work in SMA mice revealed upper MN vulnerability\, indicating SMA pathogenesis is far more complex than classically conceived. We have shown that SMN deficiency infl uences cortical layering and cytoarchitecture during corticogenesis. This developmental misplacement may represent an early event that predisposes p rojection neurons to subsequent degeneration. Not all cortical neurons are equally affected: corticospinal and then callosal projection neurons emer ge as particularly vulnerable populations\, displaying both structural and survival deficits in response to SMN reduction. More recently\, by employ ing a combination of imaging\, molecular techniques\, and electrophysiolog ical characterization of cortical inhibitory neurotransmission\, we dissec ted GABAergic signaling\, metabolism\, and interneuron function in the sen sorimotor cortex.\nSpeakers:\nProfessor Alessandro Vercelli (University of Torino) LOCATION:Sherrington Building (Florence Buchanan Lecture Theatre )\, off P arks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/c069ece9-41a1-46ee-b871-da5956ff1bcb/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Cortical alterations in Spinal Muscular Atrophy - Profess or Alessandro Vercelli (University of Torino) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Formation of common frameworks of cortical neural circuits based o n the molecular bases of neuronal migration and collateral formation - Pro fessor Makoto Sato (The University of Osaka) DTSTART;VALUE=DATE-TIME:20251204T110000Z DTEND;VALUE=DATE-TIME:20251204T120000Z UID:https://talks.ox.ac.uk/talks/id/bf37b319-1ac6-425b-bd73-0c569b36283d/ DESCRIPTION:We explore the structural mechanisms of brain function\, with a focus on neuronal migration during cerebral cortex development and the r ole of the cytoskeleton. It highlights periventricular nodular heterotopia —a genetic disorder caused by mutations in filamin A—and introduces FI LIP (filamin A interacting protein\, FILIP1 for human)\, a molecule that d egrades filamin A. Mutations in FILIP1 are linked to a spectrum of congeni tal disorders collectively termed FILIP1 disease. The study also presents new methods for visualizing neural circuits at the single-cell level\, rev ealing early axonal targeting patterns that may inform future strategies f or repairing disrupted neural networks. Unpublished findings and ongoing i nvestigations into cytoskeletal regulation and neuropsychiatric implicatio ns are included.\nSpeakers:\nProfessor Makoto Sato (The University of Osak a) LOCATION:Sherrington Building (Florence Buchanan Lecture Theatre )\, off P arks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/bf37b319-1ac6-425b-bd73-0c569b36283d/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Formation of common frameworks of cortical neural circuit s based on the molecular bases of neuronal migration and collateral format ion - Professor Makoto Sato (The University of Osaka) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Reprogrammed neurons and oligodendrocytes for brain repair after s troke - Professor Zaal Kokaia (Lund University\, Sweden) DTSTART;VALUE=DATE-TIME:20251211T160000Z DTEND;VALUE=DATE-TIME:20251211T170000Z UID:https://talks.ox.ac.uk/talks/id/3429bf22-f963-461d-b894-9fb026ce9519/ DESCRIPTION:Stroke is currently the third leading cause of disability-adju sted life-years and mortality worldwide. As the risk of stroke increases s harply with age\, incidence\, and prevalence are expected to rise even fur ther because of an aging population. This disease affects about 3.5 millio n people in the EU\, with 700 000 new cases yearly. More than half of the patients suffer significant residual impairments\, causing huge economic a nd societal burdens. Acute clinical intervention\, typically involving sur gical removal or dissolution of the clot through the administration of tis sue plasminogen activator (tPA)\, aims to restore blood flow to the affect ed brain areas and is only possible within a very short time window after stroke onset. Stem cell therapy using human induced pluripotent stem (iPS) cell-derived neural precursors is a promising future therapy for stroke p atients. Two main mechanisms have been proposed to give rise to improved f unctional recovery in animal models of stroke after the transplantation of these cells. First\, the ”bystander” effect\, which could modulate th e inflammatory environment by releasing different factors from grafted cel ls\, resulting in moderate improvements in the outcome of the insult. Seco nd\, the neuronal replacement and functional integration of grafted cells into the impaired brain circuitry. This will ultimately result in optimum long-term structural and functional repair. Our data show that human skin- derived cortical progenitors can be reprogrammed to differentiate into cor tical projection neurons and functionally integrate (forming afferent and efferent synaptic connections) not only into stroke-damaged rat cortical n etworks but also into organotypic cultures of the adult human cortex. The grafted cortical neurons respond to sensory stimulation in live animals an d\, importantly\, also affect spontaneous behavior when inhibited by optog enetic stimulation. Stroke results in the loss of oligodendrocytes and axo nal demyelination\, contributing to functional impairment. Additionally\, for grafted neurons to become functional\, their axons must be myelinated. Our data show that human iPS cell-derived cells can also be reprogrammed to differentiate into functional\, bona fide oligodendrocytes. The generat ed cells exhibit the structural\, molecular\, and functional characteristi cs of mature human oligodendrocytes. They can wrap both grafted human cell - and host-derived axons from cortical neurons in different set-ups\, afte r xenotransplantation into rat stroke-injured somatosensory cortex and the human adult cortical organotypic system. Our findings raise the possibili ty that injured neural circuitry might be restored by stem cell transplant ation also in humans with stroke\, which would have major clinical implica tions. \nSpeakers:\nProfessor Zaal Kokaia (Lund University\, Sweden) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/3429bf22-f963-461d-b894-9fb026ce9519/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Reprogrammed neurons and oligodendrocytes for brain repai r after stroke - Professor Zaal Kokaia (Lund University\, Sweden) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Multi-regional neocortical dynamics underlying learning and predic tion - Dr Shuting Han (Brain Research Institute\, University of Zurich) DTSTART;VALUE=DATE-TIME:20251014T100000 DTEND;VALUE=DATE-TIME:20251014T110000 UID:https://talks.ox.ac.uk/talks/id/8c9a9b74-d5a5-4f86-bb17-252dbd7c5610/ DESCRIPTION:\nSpeakers:\nDr Shuting Han (Brain Research Institute\, Univer sity of Zurich) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/8c9a9b74-d5a5-4f86-bb17-252dbd7c5610/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Multi-regional neocortical dynamics underlying learning a nd prediction - Dr Shuting Han (Brain Research Institute\, University of Z urich) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Compulsive Reward-Seeking: Roles for Dopamine\, Synaptic Plasticit y\, and Stress - Dr Talia Lerner (Northwestern University) DTSTART;VALUE=DATE-TIME:20251028T160000Z DTEND;VALUE=DATE-TIME:20251028T170000Z UID:https://talks.ox.ac.uk/talks/id/6a849b3d-838e-4c98-b41b-aae5ac771e17/ DESCRIPTION:Compulsive behavior is a hallmark of substance use disorder an d other addictive disorders. My lab models compulsive behavior in mice usi ng a reinforcement training paradigm (RI60) that leads to habitual and pun ishment-resistant reward-seeking. By using fiber photometry and optogeneti cs to measure and manipulate dopamine signals in vivo as compulsive behavi or emerges\, we are revealing how dopamine contributes to this addiction-r elevant process. I will present published and unpublished work identifying the specific spatiotemporal features of dopamine signaling that drive com pulsion\, including evidence that adolescent stress – an important risk factor for addiction – reshapes key features of dopamine engagement in c ompulsion. These findings highlight the synaptic- and circuit-level mechan isms by which developmental experiences alter vulnerability to addiction a nd suggest new avenues for personalized treatment strategies.\nSpeakers:\n Dr Talia Lerner (Northwestern University) LOCATION:Virtual (Please contact events@dpag.ox.ac.uk for Teams Link) TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/6a849b3d-838e-4c98-b41b-aae5ac771e17/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Compulsive Reward-Seeking: Roles for Dopamine\, Synaptic Plasticity\, and Stress - Dr Talia Lerner (Northwestern University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Competition in brain development and a novel approach to neural co ding - Professor Michael Stryker (University of California) DTSTART;VALUE=DATE-TIME:20251013T130000 DTEND;VALUE=DATE-TIME:20251013T140000 UID:https://talks.ox.ac.uk/talks/id/3fffeec7-278c-4aa8-ac67-4b69c8260240/ DESCRIPTION:Inputs from the two eyes appear to compete with each other for driving responses in the developing visual cortex: occluding one eye all ows the other to become more powerful. Competition for a limited supply of neurotrophins was proposed as the cellular and molecular basis of this in teraction. We have used genetic and chemical-genetic manipulations to deli neate the mechanisms of such competition and conclude that it is the resul t of the interaction of distinct mechanisms that are not inherently compet itive.\n\nWe have also devised a novel approach to revealing the neural co de at different levels of the mouse visual system. Neural encoding manifol ds that we create can also be used to probe machine learning networks like those used to recognize pictures in Facebook. We find that these artific ial “neural” networks are more similar to big retinas than to small br ains.\n\nSPEAKER BIOGRAPHY\n\nMichael Stryker studied at Deep Springs Coll ege and the University of Michigan\, where he earned the B.A. in philosoph y with a minor in mathematics and worked in the laboratory of James Olds. He earned the Ph.D. in Peter Schiller's laboratory at M.I.T. in 1975\, fol lowed by postdoctoral research with David Hubel and Torsten Wiesel at the Harvard Medical School. He joined the Physiology Department and nascent ne uroscience program at UCSF as an assistant professor in 1978\, holds the W .F. Ganong Chair of Physiology at UCSF\, and serves on the Board of Direct ors of the Allen Institute He has been honored by the W. Alden Spencer Pri ze from Columbia\, the Ralph W. Gerard Prize from the Society for Neurosci ence\, and by election to the American Academy of Arts and Sciences and th e U.S. National Academy of Sciences.\n\nHis laboratory’s research focuse s the role of neural activity in the development and plasticity of precise connections within the central nervous system. Most of his work has been on the visual system\, in recent years on the visual cortex of the mouse. Current experiments seek to understand the cellular and neural circuit mec hanisms of activity-dependent cortical plasticity\, the interactions betwe en neural activity and molecular cues in the formation of cortical maps\, the difference between the limited plasticity in the adult brain and the m uch greater plasticity during critical periods in early life\, and novel m athematical means for understanding cortical coding. His experiments take advantage of transgenic mice and optical as well as electrical approaches for recording from and labeling and perturbing connections of specific cel ls.\nSpeakers:\nProfessor Michael Stryker (University of California) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/3fffeec7-278c-4aa8-ac67-4b69c8260240/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Competition in brain development and a novel approach to neural coding - Professor Michael Stryker (University of California) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:The regulation of neural stem cell quiescence by a physical niche - Professor Isabel Farinas (University of Valencia) DTSTART;VALUE=DATE-TIME:20250924T120000 DTEND;VALUE=DATE-TIME:20250924T130000 UID:https://talks.ox.ac.uk/talks/id/aab09393-8301-4710-afcf-cdb8f8d09189/ DESCRIPTION:1Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED)\, 2Departamento de Biología Celular\, Biol ogía Funcional y Antropología Física\, 3Instituto de Biotecnología y B iomedicina (BioTecMed)\, Universidad de Valencia\, 46100 Burjassot\, Spain .\n \nNew neurons for highly plastic olfactory circuits are produced in th e subependymal zone (SEZ) of the adult mammalian brain. Neural stem cells (NSCs) in this niche have access to a wide range of regulatory signals tha t promote continuous lifelong neurogenesis while preserving the stem cell pool. NSCs derive from radial glial cells\, which are the primary embryoni c progenitor type in the vertebrate brain\, and inherit from them part of their transcriptional program\, a bipolar elongated morphology with apico- basal polarity that allows for unique interactions with neighboring cell t ypes\, and markers associated with the astrocytic lineage. In contrast to their fetal counterparts\, most adult NSCs remain in a quiescent state und er physiological conditions. It is now widely accepted that NSCs in the SE Z exist in at least three states: quiescent (q)\, quiescent but prone to a ctivation or primed (p)\, and activated (a)\, each characterized by unique and distinct transcriptional profiles. Transitions between states likely involve significant changes in cellular physiology tightly regulated by bo th intrinsic and extrinsic factors. We have found that entry into quiescen ce is associated with the deposition of specific extracellular matrix comp onents and that adhesion to the matrix produced in response to pro-quiesce nt signals alone can induced a quiescent-like state in proliferative NSCs. This entry into quiescence depends on the RhoA-associated kinase ROCK and yes-associated protein (YAP) transcriptional activity. YAP/TAZ deletion i n NSCs leads to the loss of ECM deposition and quiescence in vivo suggesti ng that they regulate the physical niche and a quiescence-associated gene expression program in response to mechanical cues. \nSpeakers:\nProfessor Isabel Farinas (University of Valencia) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/aab09393-8301-4710-afcf-cdb8f8d09189/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:The regulation of neural stem cell quiescence by a physic al niche - Professor Isabel Farinas (University of Valencia) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Human-specific genetic modifiers underlying cortical circuit evolu tion - Professor Franck Polleux (Columbia University) DTSTART;VALUE=DATE-TIME:20250925T110000 DTEND;VALUE=DATE-TIME:20250925T120000 UID:https://talks.ox.ac.uk/talks/id/d41d3f0a-5900-4ab8-b706-ebc38c4caa3e/ DESCRIPTION:Two of the most striking features distinguishing human cortica l pyramidal neurons (CPNs) from other mammals which are thought to play a role in the emergence of our unique cognitive abilities are: (1) human CPN s receive significantly more excitatory and inhibitory synapses than any o ther mammalian species including non-human primates and (2) synaptic devel opment is strikingly neotenic in humans\, taking years to reach maturation compared to weeks or months in other mammalian species. Our lab identifie d two human-specific gene duplications called SRGAP2B/C which\, by inhibit ing all known functions of the ancestral postsynaptic protein SRGAP2A\, le ads to slower (neotenic) rates of excitatory (E) and inhibitory (I) synapt ic maturation and increased E and I synapse number (Charrier et al. Cell 2 012\; Fossatti et al Neuron 2016). We demonstrated that induction of expre ssion of human-specific genes SRGAP2B/C in mouse CPNs increases specifical ly the number of cortico-cortical synaptic connections they receive leadin g to changes in the coding properties of these neurons in vivo as well as improved behavioral performance in a sensory discrimination task (Schmidt et al. Nature 2021). I will also present recent evidence demonstrating the function of human-specific SRGAP2B/C in human neurons as key mediators of synaptic neoteny\, using a novel xenotransplantation model\, in collabora tion with Pierre Vanderhaeghen’s lab (Libé-Philippot et al. Neuron 2024 ). These results also provide the first evidence that human-specific genes such as SRGAP2B/C are not only relevant to understand human brain evoluti on but also constitute human-specific disease modifiers. \nI will also pre sent new results demonstrating that human-specific SRGAP2B/C genes also ac t as master regulators of the timing of structural and functional maturati on of microglial cells using both humanized mouse models and SRGAP2B/C los s-of-function approaches using human iPSC-derived microglia xenotransplant ation in mouse neonatal cortex. Our results demonstrate that SRGAP2B/C-dep endent induction of neotenic maturation of microglial cells participates n on-cell autonomously to the delayed timing of synaptic maturation in corti cal pyramidal neurons. Our results reveal that\, during human brain evolut ion\, human-specific genes SRGAP2B/C coordinated the emergence of neotenic features of synaptic development by acting as genetic modifiers in both n eurons and microglia.\n\nSPEAKER BIOGRAPHY\n\nSince 2013\, Franck Polleux is a Professor of Neuroscience at Columbia University and a Principal Inve stigator at the Zuckerman Mind Brain Behavior Institute in New York. He ob tained his PhD in 1997 at Université Claude Bernard in Lyon France under the supervision of Henry Kennedy and Colette Dehay. He then did his postdo ctoral training with Anirvan Ghosh at Johns Hopkins University. From 2002- 2010\, he started his independent research career at UNC-Chapel Hill\, the n moved to Scripps Research Institute in La Jolla\, CA. \nThroughout his s cientific career spanning three decades\, Dr Polleux has focused on the id entification of novel cellular and molecular mechanisms underlying the dev elopment and function of synapses\, neurons and circuits in the mammalian neocortex. More recently\, his lab started studying the genetic basis of h uman brain evolution by focusing on the role of human-specific gene duplic ations as genetic modifiers of synaptic connectivity\, circuit function an d their impact on cognition. His work demonstrates that human-specific gen es such as SRGAP2B/C not only represent human-specific modifiers of brain development but also represent unique human-specific disease modifiers in the context of neurodevelopmental disorders such as autism spectrum disord ers. In collaboration with the lab of Attila Losonczy\, he recently starte d to study the synaptic and molecular basis of feature selectivity of plac e cell emergence using mouse CA1 hippocampal pyramidal neurons as a model. \nFor his numerous scientific contributions\, he was awarded several prest igious awards such as the Albert L. Lehninger Research Prize for postdocto ral research\, the 2005 NARSAD Young Investigator Award\, the 2015 Foundat ion Roger De Spoelberch Prize\, a 2021 Nomis Foundation Award and the 2021 R35 Research Program Award\, a career award from the NIH-National Institu te of Neurological Disorders and Stroke (NINDS).\nSpeakers:\nProfessor Fra nck Polleux (Columbia University) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/d41d3f0a-5900-4ab8-b706-ebc38c4caa3e/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Human-specific genetic modifiers underlying cortical circ uit evolution - Professor Franck Polleux (Columbia University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Claustrum-Mediated Variability in the Prefrontal Cortex and Adapti ve Optics for 3 Photon Imaging - Huriye Atilgan (DPAG\, University of Oxfo rd) DTSTART;VALUE=DATE-TIME:20250723T143000 DTEND;VALUE=DATE-TIME:20250723T153000 UID:https://talks.ox.ac.uk/talks/id/3d4e3446-ae88-4ab0-a6aa-93da3b1421a0/ DESCRIPTION:Understanding how deep brain structures like the claustrum sha pe cortical dynamics requires both mechanistic insight and technical innov ation. In the first part of this talk\, I will present recent findings on how the claustrum modulates neuronal dynamics in the dorsal prefrontal cor tex (dPFC). Using two-photon calcium imaging combined with optogenetic sti mulation of claustrum axons\, we identified distinct neuronal subpopulatio ns with altered responsiveness to combined visual and optogenetic inputs. Claustrum activation enhanced both neural variability and network homogene ity — effects that persisted during Pavlovian training. Silencing experi ments further revealed that the claustrum may operate bidirectionally to m aintain elevated variability and coordinated activity in the dPFC. In the second part\, I will introduce a practical adaptive optics-assisted three- photon (3P) imaging system developed to enable deep functional imaging in behaving mice. Motivated by the challenge of imaging the claustrum\, we im plemented a three-tier correction strategy targeting aberrations from the microscope\, cranial window\, and tissue. This approach significantly impr oved resolution and signal quality across distinct cortical regions and wi ll support direct imaging of the claustrum and other deep brain structures in future studies.\n\nSPEAKER BIOGRAPHY\n\nDr. Huriye Atilgan is a Sir He nry Wellcome Fellow in the Lak Lab. Her research focuses on how sensory in formation is transformed into internal neural representations that guide l earning\, decision-making\, and action. She combines behavioral paradigms with advanced optical imaging techniques — including two-photon and thre e-photon microscopy with adaptive optics — to study the dynamics of neur al circuits in the prefrontal cortex and deep brain regions such as the cl austrum. Huriye completed her PhD in Auditory Neuroscience at University C ollege London in the lab of Professor Jennifer Bizley\, where she investig ated multisensory integration and auditory scene analysis. She then pursue d postdoctoral training in Alex Kwan’s lab at Yale University\, focusing on the role of the medial prefrontal cortex in value-based decision-makin g. She joined the University of Oxford in 2020\, where she has since led p rojects on claustrum-prefrontal interactions and developed deep imaging me thodologies to enable high-resolution recordings during behavior. Her work has been recognized with numerous fellowships and awards\, and she contin ues to contribute to both fundamental neuroscience and the development of novel experimental approaches.\nSpeakers:\nHuriye Atilgan (DPAG\, Universi ty of Oxford) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/3d4e3446-ae88-4ab0-a6aa-93da3b1421a0/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Claustrum-Mediated Variability in the Prefrontal Cortex a nd Adaptive Optics for 3 Photon Imaging - Huriye Atilgan (DPAG\, Universit y of Oxford) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Towards using large-scale\, cross-brain neuronal recordings to ide ntify the brain’s internal signals - Professor Carlos Brody (Princeton U niversity) DTSTART;VALUE=DATE-TIME:20250612T130000 DTEND;VALUE=DATE-TIME:20250612T140000 UID:https://talks.ox.ac.uk/talks/id/9bb72f13-a98d-4c06-a336-d1fb939bc069/ DESCRIPTION:Using large-scale recordings from frontal decision-making regi ons in rats performing a perceptual decision-making task\, we recently dis covered an internally-timed signal\, coordinated across simultaneously rec orded neurons\, that indicates the moment when the subject makes up their mind\, or in other words\, commits to a decision. This moment\, which we r efer to as “nTc”\, for “Neurally-inferred Time of Commitment\,” ca n occur covertly\, many hundreds of milliseconds before\, and independentl y of\, the moment when the subject overtly reports their decision. In a fu rther set of experiments\, using 8 Neuropixels probes to record from thous ands of neurons in tens of brain regions simultaneously across the brain\, we discovered that decision-related neural activity is tightly coordinate d across brain regions. Remarkably\, the activity coordination across thes e regions\, and across both hemispheres\, is dominated by a single one-dim ensional variable. Furthermore\, the frontally-defined nTc marks a major s tate change in decision-related neural activity across the brain: in all r ecorded regions\, choice-prediction accuracy abruptly stops growing\, and cross-region coordination drops drastically\, after nTc. This suggests tha t detection of nTc\, a purely internal\, neurally defined moment\, will be critical for appropriately parsing decision-related neural activity into states with entirely different functional properties and significance. Goi ng beyond decision-making\, we point out that the overwhelming bulk of var iance in neural activity is of unknown origin or meaning\, yet is known to be structured across neurons. This is exactly what nTc looked like before we discovered it. We propose that\, similar to nTc\, most neural activity may consist of internally-timed and internally-defined signals. Such sign als would induce structure in neural activity across neurons yet\, if thei r timing and characteristics are unknown\, would otherwise look like noise . We further propose that modern AI techniques\, combined with large-scale recordings\, provide unprecedented opportunities to detect\, parse\, and characterize that structure. We believe this characterization will provide fundamental clues towards understanding internal signals and thus towards elucidating the inner conversation of the mind.\n\nSPEAKER BIOGRAPHY\n\nB orn and raised in Mexico City\, Carlos Brody did his Ph.D. in the Computat ion and Neural Systems Program at Caltech. He then did a postdoc in Ranulf o Romo's lab in Mexico\, analyzing and modeling data from monkeys performi ng working memory and decision-making tasks. This was followed by a short postdoc at NYU in Tony Movshon's lab\, after which he took his first facul ty position at Cold Spring Harbor Labs\, working in computational neurosci ence. After a few years at CSHL\, he started doing experiments with behavi ng rats. He then moved to Princeton University\, where his lab pursues bot h computational and experimental neuroscience. Brody is an Investigator of the Howard Hughes Medical Institute.\nSpeakers:\nProfessor Carlos Brody ( Princeton University) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/9bb72f13-a98d-4c06-a336-d1fb939bc069/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Towards using large-scale\, cross-brain neuronal recordin gs to identify the brain’s internal signals - Professor Carlos Brody (Pr inceton University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Dopamine and Movement: Defining Timescales of Modulation - Dr Nico las Tritsch (Faculty of Medicine and Health Sciences\, McGill University\, Canada) DTSTART;VALUE=DATE-TIME:20250610T103000 DTEND;VALUE=DATE-TIME:20250610T113000 UID:https://talks.ox.ac.uk/talks/id/7a433406-e786-478f-a36c-11233456d5fb/ DESCRIPTION:Ever since the discovery that the degeneration of midbrain DA neurons (mDANs) projecting to the striatum underlies bradykinesia (i.e.\, slowness of movement) in Parkinson’s disease (PD)\, DA has become synony mous with motor vigor. However\, the mechanisms through which DA contribut es to the speed and amplitude of individual voluntary movements are still debated. Initial investigations suggested a somewhat slow or permissive ro le for DA\, but recent experiments in rodents proposed a stronger and fast er role for DA in the dynamic control of the gain of motor commands. In th is presentation\, I will describe our attempts at better understanding how dopamine contributes to motor vigor through the study of release patterns \, lesions\, and optogenetic and pharmacological manipulations. Our findin gs call into question the widely-held view that phasic fluctuations in ext racellular dopamine control the vigor of ongoing movements\, constraining the kinds of mechanisms and timescales that dopamine likely acts on to mod ify behavior.\nSpeakers:\nDr Nicolas Tritsch (Faculty of Medicine and Heal th Sciences\, McGill University\, Canada) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/7a433406-e786-478f-a36c-11233456d5fb/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Dopamine and Movement: Defining Timescales of Modulation - Dr Nicolas Tritsch (Faculty of Medicine and Health Sciences\, McGill Uni versity\, Canada) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Dissecting the synaptic basis of learning in vivo - Dr William (Ja ke) Wright (University of California\, San Diego) DTSTART;VALUE=DATE-TIME:20250619T160000 DTEND;VALUE=DATE-TIME:20250619T170000 UID:https://talks.ox.ac.uk/talks/id/596a263b-8eb4-4f0b-9275-a6aecba5761d/ DESCRIPTION:The ability to acquire and adapt behavior through the process of learning is one of the most fundamental functions of the brain and\, wh en gone awry can lead to numerous disorders. Synaptic plasticity is though t to underlie learning by altering the input-output transformations perfor med by individual neurons and reorganize neural circuits. Dr. Wright will discuss his recent findings dissecting how synaptic plasticity is regulate d in the intact brain during learning to produce new behaviors.\n\nSPEAKER BIOGRAPHY\n\nDr. William (Jake) Wright is a postdoctoral fellow in the la b of Dr. Takaki Komiyama at the University of California\, San Diego (UCSD ). He currently investigates how synaptic plasticity is regulated in the i ntact brain and how this plasticity in turn reorganizes neural circuits to mediate learning. Prior to joining the Komiyama lab at UCSD\, Dr. Wright received his PhD in neuroscience from the University of Pittsburgh\, where he worked with Dr. Yan Dong to study the synaptic mechanisms underlying d rug-associated memories. \nSpeakers:\nDr William (Jake) Wright (University of California\, San Diego) LOCATION:Virtual (Please contact events@dpag.ox.ac.uk for Teams Link) TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/596a263b-8eb4-4f0b-9275-a6aecba5761d/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Dissecting the synaptic basis of learning in vivo - Dr Wi lliam (Jake) Wright (University of California\, San Diego) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Role of subplate neurons in the development and evolution of the m ammalian neocortex - Professor Chiaki Ohtaka-Maruyama (Developmental Neuro science Project\, Tokyo Metropolitan Institute of Medical Science\, Tokyo\ , Japan) DTSTART;VALUE=DATE-TIME:20250603T160000 DTEND;VALUE=DATE-TIME:20250603T170000 UID:https://talks.ox.ac.uk/talks/id/06727ab4-b25d-444d-96b7-cf832ea3803e/ DESCRIPTION:In the mammalian neocortex\, an enormous number of neurons are precisely arranged in an ordered 6-layered structure in an inside-out man ner. This structure is formed by the sequential generation of neurons and their migration toward the brain surface\, termed radial neuronal migratio n. In order to complete the neocortical layer structure within the limited time period of embryogenesis\, the radial migration process must be contr olled precisely and efficiently. We previously reported that subplate neur ons (SpNs)\, one of the firstborn and matured types of neurons in the deve loping neocortex\, play an important role in regulating radial migration. In addition to controlling radial neuronal migration\, the subplate (SP) l ayer is essential in establishing thalamocortical connections and plays a critical role in embryonic cortex formation. Primates such as monkeys and humans have a transiently highly expanded SP layer during the embryonic pe riod compared to mice. However\, its biological significance and the molec ular mechanisms responsible for this expansion still need to be understood . We aimed to elucidate the mechanism by performing Visium and Xenium spat ial transcriptomic analysis using the embryonic cerebrum of marmosets and humans. By comparing these data with mouse data\, we identified genes spec ifically expressed in the SP layer of the primate. I will discuss the cand idate genes identified in this analysis and the role of the SP layer in th e evolution of the mammalian brain.\nSpeakers:\nProfessor Chiaki Ohtaka-Ma ruyama (Developmental Neuroscience Project\, Tokyo Metropolitan Institute of Medical Science\, Tokyo\, Japan) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/06727ab4-b25d-444d-96b7-cf832ea3803e/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Role of subplate neurons in the development and evolution of the mammalian neocortex - Professor Chiaki Ohtaka-Maruyama (Developmen tal Neuroscience Project\, Tokyo Metropolitan Institute of Medical Science \, Tokyo\, Japan) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Development of Motion Vision - Associate Professor Kristina Nielse n (Johns Hopkins University) DTSTART;VALUE=DATE-TIME:20250501T150000 DTEND;VALUE=DATE-TIME:20250501T160000 UID:https://talks.ox.ac.uk/talks/id/649366f9-6e14-4e8f-be1f-ea518508b922/ DESCRIPTION:Development of Motion Vision\nSpeakers:\nAssociate Professor K ristina Nielsen (Johns Hopkins University) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/649366f9-6e14-4e8f-be1f-ea518508b922/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Development of Motion Vision - Associate Professor Kristi na Nielsen (Johns Hopkins University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Special Neuroscience Seminar: Introduction to University of Debrec en\, Hungary - Various Speakers DTSTART;VALUE=DATE-TIME:20250218T150000Z DTEND;VALUE=DATE-TIME:20250218T170000Z UID:https://talks.ox.ac.uk/talks/id/5c7a70b8-5048-4f65-b71a-d2b08e1098ef/ DESCRIPTION:15:00 - Prof. Dr. József Tőzsér (Vice Rector of Sectoral De velopment Responsible for Life Sciences) – Short introduction of the Uni versity of Debrecen (Hungary)\n\n15:20 - Prof. Dr. László Mátyus (Dean\ , Faculty of Medicine) – Research Focus of the Faculty of Medicine\n\nMe dical education has a long tradition in Debrecen\, it started on October 2 3\, 1918. Today besides medicine\, the Faculty teaches molecular biologist s\, health psychologist and medical diagnostic analysts. Medicine and mole cular biology courses are available for foreign students as well in separa te course where the medium of instruction is English. Around 4000 students are enrolled currently in these courses.\nResearch and education is carri ed out in 22 departments of basic sciences and in 25 clinical departments\ , by more than 500 faculty members. Research is also organized by doctoral schools. The Faculty hosts several research groups financed by the Hungar ian Research Network. Around ten Core Facilities support our research acti vities.\nA brief introduction about the main research foci of the Faculty of Medicine will be presented.\n\n15:40 - Dr. Péter Szücs (Director\, De partment of Anatomy\, Histology and Embryology) - Normal and pathological nociceptive processing in the spinal dorsal horn.\n\nThe talk will summari ze the main research lines of the "Spinal nociceptive processing" workgrou p of the Department of Anatomy\, Histology\, and Embryology (UD). \nFrom a natomical techniques that help describing wiring to electrophysiological a nd optogenetic approaches used to resolve function\, the talk will showcas e the facilities and methods utilized by researchers of the department. Re cent findings on spinal dorsal horn neuron morphology\, interneuronal netw orks\, diabetic neuropathy and neuroinflammation will be presented.\n\n16: 00 - Dr. Zoltán Mészár (Assistant Professor\, Department of Anatomy\, H istology and Embryology) - Molecular dissection of spinal dorsal horn neur ons involved in nociception\; from neurodevelopment to neuromodulation\n\n The dorsal horn of the spinal cord serves as the initial relay station for sensory information\, particularly pain perception. As a crucial target f or pain relief and modulation\, it contains a spinal pain processing netwo rk composed of morphologically\, functionally\, and neurochemically divers e neurons. Our research focuses on this area and the ascending spinal circ uits\, examining their development\, potential intervention points\, and n etwork modifications using transgenic mouse models. Neurons in the dorsal horn are born during a specific interval\, followed by their migration to form the laminae of Rexed\, which exhibit distinct morphological character istics specific to each neuron type. Despite their functional and morpholo gical diversity\, these neurons originate from a single progenitor pool. O ur studies indicate that extracellular matrix (ECM) macromolecules play a significant role in this structural transformation. Functionally\, even th ough the neurons are heterogeneous\, they respond differently to various t ypes of stimuli. We discovered that dynorphin-expressing neurons significa ntly contribute to the transmission of pain resulting from burn injuries. By manipulating these cells using CRISPR/Cas9 technology\, we found that t he heat-induced pain threshold in mice changes significantly. Recent RNAse q studies suggest that Wnt signaling may significantly contribute to the c hronicization of heat-induced pain.\n\n16:20 Prof. Dr. József Tőzsér (V ice Rector of Sectoral Development Responsible for Life Sciences) - Common features and differences of retroviral and SARS-CoV proteases\n\nThe seve re acute respiratory syndrome coronaviruses include the human pathogenic S ARS-CoV-2 that has been responsible for a global pandemic since its emerge nce in 2019. Human immunodeficiency virus type-1 (HIV-1) that belongs to t he lentivirus genus of Retroviridae family is continuously infecting human s since the 1980s. Both type of viruses are using RNA genomes that confer high mutational capacities that lead to rapid evolution of the viruses\, a s well as quick emergence of resistance to any drugs developed against the viral proteins. Both viruses utilize viral proteases to process the viral polyproteins\, and these enzymes - especially the HIV-1 protease and the SARS-CoV-2 main protease (Mpro) - have been successfully targeted by ratio nally designed drugs\, as the polyprotein processing is an essential step of viral replication in both cases. The first HIV protease inhibitor (saqu inavir) was approved by the Food and Drug Administration (FDA) in 1995\, f ollowed later by the release of eight additional therapeutic protease inhi bitors. In 2022\, the first protease inhibitor that was fully approved for the treatment of COVID-19 patients was Paxlovid. This drug contains the H IV-1 protease inhibitor ritonavir as a pharmacokinetic enhancer\, while th e main component is nirmatrelvir\; which is a reversible covalent inhibito r of SARS-CoV-2 Mpro. Although HIV-1 protease and SARS-CoV-2 Mpro are usin g completely different catalytic mechanisms\, and have distinct structural characteristics\, the protease functions\, their self-processing route\, as well as resistance development show striking similarities. It is known from the almost 40-year history of the antiretroviral therapies that virus es can escape the selective drug-induced pressure by developing resistance mutations. Only a few SARS-CoV-2 Mpro inhibitors have been approved to da te\, mostly under emergency conditional authorization\, therefore\, the mo notherapeutic settings might potentially increase the risk for resistance development. Therefore\, the knowledge on HIV-1 and other retroviral prote ases can substantially help the fight against SARS coronaviruses. \nProje ct no. TKP2021-EGA-20 has been implemented with the support provided by th e Ministry of Culture and Innovation of Hungary from the National Research \, Development and Innovation Fund\, financed under the TKP2021-EGA fundin g scheme. Supported by the University of Debrecen (UD) Program for Scienti fic Publication\, by the UD Faculty of Medicine Research Fund (Bridging fu nd)\, and by UD Scientific Research Bridging Fund (DETKA) and by NKFIH Adv anced 150532 Grant. János A. Mótyán is a receiver of János Bolyai Rese arch Scholarship of the Hungarian Academy of Sciences (BO/00110/23/5)\, wh ile Gyula Hoffka is supported by the University Research Fellowships progr am (EKÖP-24-4-I-DE-435). \n\n16:40 Orsolya Gregán (Director\, Centre for International R&D Relations) – Financial Opportunities for Cooperation between the University of Oxford and the University of Debrecen\n\nThis pr esentation explores the available financial opportunities for fostering co llaboration between the University of Oxford and the University of Debrece n. Given the current restrictions on Erasmus+ and Horizon Europe funding f or both institutions\, alternative sources must be considered. Potential f unds\, including national and bilateral research grants such as the HU-RIZ ONT Programme and mobility support of the Pannónia Program will be higlig hted. Additionally\, opportunities from private foundations\, industry par tnerships\, and internal university funding will be discussed. By leveragi ng these resources\, both institutions can establish sustainable research collaborations\, support mobility programs\, and enhance academic exchange . The session will provide insights into navigating funding challenges and identifying strategic opportunities for long-term cooperation.\nSpeakers: \nVarious Speakers LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/5c7a70b8-5048-4f65-b71a-d2b08e1098ef/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Special Neuroscience Seminar: Introduction to University of Debrecen\, Hungary - Various Speakers TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:From Stem Cells to Assembloids to Constructing Human Neural Circui ts to Study Development and Disease - Professor Sergiu P. Pașca (Stanfor d University) DTSTART;VALUE=DATE-TIME:20250220T160000Z DTEND;VALUE=DATE-TIME:20250220T170000Z UID:https://talks.ox.ac.uk/talks/id/d96ed0ef-9299-4b7c-8917-919c9a540e8e/ DESCRIPTION:A critical challenge in understanding the programs underlying the development\, assembly and dysfunction of the human brain is the lack of direct access to intact\, functioning human brain tissue for direct inv estigation and manipulation. In this talk\, I will describe efforts in my laboratory to build functional cellular models and to capture previously i naccessible aspects of human brain development and dysfunction. To achieve this\, we have pioneered the use of instructive signals to derive\, from pluripotent stem cells\, self-organizing 3D tissue structures called regio nalized neural organoids that resembles domains of the developing central nervous system. We have shown that these cultures\, such as the ones resem bling the cerebral cortex\, recapitulate many features of neural developme nt\, can be derived with high reliability across dozens of cell lines and experiments\, and can be maintained for years in vitro to capture advanced stages of neural and glial maturation and function. To model complex cell -cell interactions\, we introduced assembloids and demonstrated their use in modeling cell migration\, formation of neural circuits and disease proc esses. To advance maturation and circuit integration of organoids\, we int roduced a transplantation paradigm and demonstrated that engrafted human n eurons can respond to sensory stimulation in the animal and can drive rewa rd-seeking behavior therefore enabling behavioral readouts from patient-de rived cells. Lastly\, I will illustrate how these methods can be combined with modern neuroscience tools to study neuropsychiatric disorders and dev elop therapeutics.\nSpeakers:\nProfessor Sergiu P. Pașca (Stanford Univer sity) LOCATION:Sherrington Building (Blakemore Lecture Theatre)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/d96ed0ef-9299-4b7c-8917-919c9a540e8e/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:From Stem Cells to Assembloids to Constructing Human Neur al Circuits to Study Development and Disease - Professor Sergiu P. Pașca (Stanford University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Cellular Models of Schizophrenia - Associate Professor Carl Sellgr en Majkowitz (Karolinska Institute\, Sweden) DTSTART;VALUE=DATE-TIME:20250203T160000Z DTEND;VALUE=DATE-TIME:20250203T170000Z UID:https://talks.ox.ac.uk/talks/id/cbbf3301-135f-4c79-a77b-c1a85eadf93e/ DESCRIPTION:The Sellgren laboratory uses models of the developing human br ain (based on induced pluripotent stem cells) to study mechanisms that gui de neurodevelopment and that are involved in different neurodevelopmental disorders (using genetic and environmental risk models). For this\, skin b iopsies are collected from patients at the psychiatric clinics in Stockhol m and integrate experimental data with observational data obtained through genetic analyses\, brain imaging\, and analyses of cerebrospinal fluid. The clinical unit foremost works within the Karolinska Schizophrenia Proje ct but also in collaboration with other cohort studies. The group have a s pecial interest in glial modulation of developing neuronal circuits and ha ve developed brain organoid models that incorporates both microglia and ol igodendrocyte lineage cells. Combined with different functional assays\, s ingle cell multiomics techniques are also commonly used in the laboratory to characterize brain organoids. \nSpeakers:\nAssociate Professor Carl Sel lgren Majkowitz (Karolinska Institute\, Sweden) LOCATION:Sherrington Building (Florence Buchanan Lecture Theatre)\, off Pa rks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/cbbf3301-135f-4c79-a77b-c1a85eadf93e/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Cellular Models of Schizophrenia - Associate Professor Ca rl Sellgren Majkowitz (Karolinska Institute\, Sweden) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Developmental Mechanisms in Schizophrenia - Professor Konstantin K hodosevich (University of Copenhagen) DTSTART;VALUE=DATE-TIME:20250203T150000Z DTEND;VALUE=DATE-TIME:20250203T160000Z UID:https://talks.ox.ac.uk/talks/id/b4bfac1b-0447-40f2-ab2b-7aeecf9df906/ DESCRIPTION:Brain development is a tremendously complex process in which a myriad of neuronal and non-neuronal cell types is generated and assembled into functional circuits in a highly organized manner. Many psychiatric d isorders arise when developmental processes are perturbed by various genet ic and environmental factors. Given high cellular diversity in the brain\, for most psychiatric disorders\, we are still far from understanding how they arise and what types of neurons and circuits underlie functional impa irments in psychiatric disorders. Recent technological advance in single-c ell analysis allowed us to address how psychiatric risk factors perturb br ain development at single-cell resolution. In my presentation\, I will sho w recently published and unpublished data from my lab\, where we implement ed single-cell analysis to identify how neuronal subtypes and their networ ks are perturbed during brain development in schizophrenia risk factor mod els\, followed up by functional experiments to validate single-cell data.\ nSpeakers:\nProfessor Konstantin Khodosevich (University of Copenhagen) LOCATION:Sherrington Building (Florence Buchanan Lecture Theatre)\, off Pa rks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/b4bfac1b-0447-40f2-ab2b-7aeecf9df906/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Developmental Mechanisms in Schizophrenia - Professor Kon stantin Khodosevich (University of Copenhagen) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Neural mechanisms for flexible and goal-directed sensorimotor tran sformations during decision-making - Dr Michael Lohse (Sainsbury Wellcome Centre\, UCL) DTSTART;VALUE=DATE-TIME:20241118T140000Z DTEND;VALUE=DATE-TIME:20241118T150000Z UID:https://talks.ox.ac.uk/talks/id/a53dfb31-1a61-4c64-9a6d-10c61d52baff/ DESCRIPTION:A hallmark of the mammalian brain is the ability to link relev ant external events to specific actions based on internal goals. \n \nIn t his talk\, I will first present recent findings revealing a brain-wide dis tributed network of areas which learns to transform sensation into action by orthogonalizing movement and deliberation population dynamics. Within t he deliberation population dynamics a sparse subset of neurons couple sens ory evidence encoding with movement preparatory dynamics.\n \nI will then present work demonstrating that this sensorimotor transformation can be fl exibly gated - based on the animals’ internal goals - by a novel functio nal frontal cortical area (located at the anterior tip of secondary motor cortex). This area exercises cognitive control by clamping striatal popula tion dynamics\, to effectively move sensory evidence dynamics in and out o f an action generating state based on the animals internal goals.\n \nToge ther\, these findings provide a brain-wide account of how sensation is tra nsformed into action and how this can be flexibly gated through a cortico- striatal clamping mechanism.\nSpeakers:\nDr Michael Lohse (Sainsbury Wellc ome Centre\, UCL) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/a53dfb31-1a61-4c64-9a6d-10c61d52baff/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Neural mechanisms for flexible and goal-directed sensorim otor transformations during decision-making - Dr Michael Lohse (Sainsbury Wellcome Centre\, UCL) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Decoding the prefrontal cortex through single cell omics - Aritra Bhattacherjee (Harvard Medical School) DTSTART;VALUE=DATE-TIME:20241119T110000Z DTEND;VALUE=DATE-TIME:20241119T120000Z UID:https://talks.ox.ac.uk/talks/id/380f5d80-e71f-4cda-87c2-4317af723a67/ DESCRIPTION:The prefrontal cortex (PFC) is a higher order cognitive center that regulates diverse functions like learning\, memory\, emotion\, rewar d\, executive function\, and even pain processing\, via a descending inhib ition on the spinal cord. Not surprisingly\, the PFC is implicated in many neurological and psychiatric disorders\, some of which are genetically in flicted\, while some are adaptive or complex. Yet\, molecular mechanisms u nderlying PFC disorders have been difficult to comprehend owing to the com plexity of cell types\, circuits and functions of this region\, making it extraordinarily challenging to contemplate specificity in therapeutic targ eting. However\, biochemical\, morphological or electrical heterogeneity o f neurons\, which underlie this complexity\, must emerge from their discre te molecular compositions. We asked whether the diversity of cell types (a nd functions) can be reconciled by mapping their transcriptomic compositio ns. Using a combination of single cell sequencing and spatial transcriptom ics (MERFISH or Multiplexed Error Robust Fluorescence in situ hybridizatio n) we decoded the remarkable molecular diversity of PFC neurons and their discrete anatomical organization patterns along the antero-posterior and d orsal-ventral axes. Distinct cellular and transcriptional features emerged \, characterizing the PFC relative to its adjoining cortical areas. Dramat ic transcriptional changes were observed across neuronal subtypes during a dolescence\, when postnatal plasticity peaks in PFC\, revealing distinct e xpression and regulation of several GWAS candidate genes for major neurops ychiatric disorders. By generating cell type specific Cre mouse lines\, we mapped neuronal subtypes and circuits underlying adaptive disorders like chronic pain and drug addiction\, in their respective disease models. We a re currently investigating the transcriptional and epigenetic changes in t hese circuits during the disease pathogenesis. Cumulatively\, our data ind icate that redefining composition and organization through single cell omi cs is greatly facilitating our understanding of the biology and pathology of the PFC and may enable precisely targeting therapies for specific disor ders in the future.\nSpeakers:\nAritra Bhattacherjee (Harvard Medical Scho ol) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/380f5d80-e71f-4cda-87c2-4317af723a67/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Decoding the prefrontal cortex through single cell omics - Aritra Bhattacherjee (Harvard Medical School) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Interpretable artificial intelligence to identify brain aging traj ectories leading to Alzheimer's disease - Associate Professor Andrei Irimi a (University of Southern California) DTSTART;VALUE=DATE-TIME:20241106T110000Z DTEND;VALUE=DATE-TIME:20241106T120000Z UID:https://talks.ox.ac.uk/talks/id/c997289d-2ab5-49ff-be2f-fe8f483c5291/ DESCRIPTION:Early estimation of disease risk from magnetic resonance image s (MRIs) can help to reduce the clinical burden of incurable neurological disorders such as Alzheimer's disease and related dementias (ADRD). Tradit ionally\, researchers' attempts to identify early biomarkers of future ADR D have relied on neuroanatomic measures defined a priori\, including brain volume loss and cortical thinning. Such measures have limited utility due to their modest sensitivity and specificity for the prognostication of AD RD. Recent progress in explainable artificial intelligence (XAI) leverages the ability of deep neural networks to find complex patterns of abnormal neuroanatomic aging that are not apparent to humans and that can better pr edict ADRD morbidity. Because brain aging is lifelong\, such abnormal agin g trajectories have the advantage of being detectable relatively early in adulthood to mitigate ADRD risk. Our patient-tailored anatomic maps of bra in aging highlight differences in neurosenescence according to sex\, decad al age group\, biometrics\, demographics\, and cognitive status. These XAI -empowered findings identify\, for the first time\, the anatomic substrate s of complex endophenotypes whose structural bases were previously thought to be undetectable by MRI. In conclusion\, XAI holds considerable potenti al to assist translational neuroscience\, to advance basic studies of brai n structure/function\, and to develop early biomarkers of ADRD risk in agi ng adults with normal cognition.\n\nSPEAKER BIOGRAPHY\n\nAndrei Irimia\, P hD is a visiting associate professor at King's College London\, currently on sabbatical from the Leonard Davis School of Gerontology at the Universi ty of Southern California. Dr. Irimia is a biogerontologist and computatio nal neurobiologist studying how (epi)genetic and environmental factors con strain brain aging in health and disease. In collaboration with the ENIGMA Consortium and with other researchers across the world\, his team uses ex plainable artificial intelligence (XAI)\, omics\, and neuroimaging to char acterize risk factors for Alzheimer's disease (AD). These methods are syne rgized with biometrics\, demographics and with large-scale research on pre -industrial populations to build XAI models that forecast AD conversion in aging adults. Such approaches relate AD risk to accelerated aging\, neuro vascular calcification\, industrialization\, urbanization\, lifestyle and traumatic brain injury. \nSpeakers:\nAssociate Professor Andrei Irimia (Un iversity of Southern California) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/c997289d-2ab5-49ff-be2f-fe8f483c5291/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Interpretable artificial intelligence to identify brain a ging trajectories leading to Alzheimer's disease - Associate Professor And rei Irimia (University of Southern California) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Insights and strategies during learning - Assistant Professor Kish ore Kuchibhotla (Johns Hopkins University) DTSTART;VALUE=DATE-TIME:20241114T103000Z DTEND;VALUE=DATE-TIME:20241114T113000Z UID:https://talks.ox.ac.uk/talks/id/173bdbe9-0554-4852-a5dc-a53bb01c3b7c/ DESCRIPTION:My lab studies the distributed mechanisms that support sensori motor learning\, with an emphasis on the role of neuromodulation and senso ry systems. In this seminar\, I will propose that re-visiting our understa nding of the shape of the learning curve and its underlying cognitive driv ers is essential for uncovering its neural basis. Rather than thinking abo ut learning as either ‘slow’ or ‘sudden’\, I will argue that learn ing is better interpreted as a combination of the two. I will provide beha vioral evidence that sensorimotor learning can be dissociated into two par allel processes: rapid\, step-like improvements in the acquisition of task knowledge\, paired with a slower and more variable process of behavioral expression\, which can be attributed to animals’ structured exploration. I will then present probabilistic optogenetic and longitudinal two-photon imaging results from mice learning an auditory go/no-go task that demonst rates a default role for the auditory cortex in task acquisition. We find dedicated neural ensembles that quickly form to encode the discriminative task contingencies\; these late-in-trial contingency signals are uncoupled from the underlying stimulus representation. Finally\, I will discuss som e ongoing work in my lab focused on the neural basis of lifelong \, multi- task learning.\nSpeakers:\nAssistant Professor Kishore Kuchibhotla (Johns Hopkins University) LOCATION:Dorothy Crowfoot Hodgkin Building (DCHB 20-026 Seminar Room 1)\, off South Parks Road OX1 3QU TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/173bdbe9-0554-4852-a5dc-a53bb01c3b7c/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Insights and strategies during learning - Assistant Profe ssor Kishore Kuchibhotla (Johns Hopkins University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Rapid emergence of latent knowledge in the sensory cortex drives l earning - Céline Drieu (Johns Hopkins University\, Baltimore) DTSTART;VALUE=DATE-TIME:20241017T140000 DTEND;VALUE=DATE-TIME:20241017T150000 UID:https://talks.ox.ac.uk/talks/id/a82626e4-3f20-43b6-b1b0-640b92d91715/ DESCRIPTION:Rapid learning confers significant advantages to animals in ec ological environments. Despite the need for speed\, animals appear to only slowly learn to associate rewarded actions with predictive cues. This slo w learning is thought to be supported by a gradual expansion of predictive cue representation in the sensory cortex. However\, evidence is growing t hat animals learn more rapidly than classical performance measures suggest \, challenging the prevailing model of sensory cortical plasticity. Here\, we investigated the relationship between learning and sensory cortical re presentations. We trained mice on an auditory go/no-go task that dissociat ed the rapid acquisition of task contingencies (learning) from its slower expression (performance). Optogenetic silencing demonstrated that the audi tory cortex (AC) drives both rapid learning and slower performance gains b ut becomes dispensable at expert. Rather than enhancement or expansion of cue representations\, two-photon calcium imaging of AC excitatory neurons throughout learning revealed two higher-order signals that were causal to learning and performance. First\, a reward prediction (RP) signal emerged rapidly within tens of trials\, was present after action-related errors on ly early in training\, and faded at expert levels. Strikingly\, silencing at the time of the RP signal impaired rapid learning\, suggesting it serve s an associative and teaching role. Second\, a distinct cell ensemble enco ded and controlled licking suppression that drove the slower performance i mprovements. These two ensembles were spatially clustered but uncoupled fr om underlying sensory representations\, indicating a higher-order function al segregation within AC. Our results reveal that the sensory cortex manif ests higher-order computations that separably drive rapid learning and slo wer performance improvements\, reshaping our understanding of the fundamen tal role of the sensory cortex. I will end by briefly discussing my broade r research questions which focus on brain-wide computations for learning a nd memory.\nSpeakers:\nCéline Drieu (Johns Hopkins University\, Baltimore ) LOCATION: Virtual (Please contact events@dpag.ox.ac.uk for Teams Link) TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/a82626e4-3f20-43b6-b1b0-640b92d91715/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Rapid emergence of latent knowledge in the sensory cortex drives learning - Céline Drieu (Johns Hopkins University\, Baltimore) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:What the hell is the dorsal striatum for? - David Robbe (Institut de Neurobiologie de la Méditerranée\, Marseille\, France) DTSTART;VALUE=DATE-TIME:20241031T150000Z DTEND;VALUE=DATE-TIME:20241031T160000Z UID:https://talks.ox.ac.uk/talks/id/0b8771fc-5517-4bdc-bd4f-83db8f6eba86/ DESCRIPTION:A well-accepted idea in systems neuroscience is that different types of memories are stored in specific brain regions or networks. Withi n this framework\, the dorsal striatum is believed to play a critical role in learning and recalling/selecting adaptive actions\, also referred to a s procedural skills. Although many studies support this view\, it is not w ithout experimental paradoxes—such as the surprisingly modest memory or decisional impairments following lesion/inactivation of the basal ganglia output nuclei. Additionally\, the strong influence of sensorimotor cortica l dynamics over striatal activity suggests that action selection might inv olve extended cortical and subcortical networks\, raising the question of the specific contribution of the dorsal striatum. In my talk\, I will pres ent work from our team (and others) supporting the view that the dorsal st riatum's contribution to action selection may be derived from its involvem ent in the motivational underpinnings of reward-oriented behaviors\, and m ore specifically\, the tendency of animals to minimize time and effort. I will discuss how such a motivational function could be relevant to underst anding brain disorders such as Parkinson's disease and depression.\nSpeake rs:\nDavid Robbe (Institut de Neurobiologie de la Méditerranée\, Marseil le\, France) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/0b8771fc-5517-4bdc-bd4f-83db8f6eba86/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:What the hell is the dorsal striatum for? - David Robbe ( Institut de Neurobiologie de la Méditerranée\, Marseille\, France) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Engrams as a substrate for information storage - Associate Profess or Tomás Ryan (Trinity College Dublin) DTSTART;VALUE=DATE-TIME:20240904T160000 DTEND;VALUE=DATE-TIME:20240904T170000 UID:https://talks.ox.ac.uk/talks/id/ea710d9d-7005-4414-8776-ce171b8fc38a/ DESCRIPTION:How is learned information stored in the brain and how does it interact with the innate representations to enable adaptive behaviour? Th e result of plasticity that accounts for a given memory can be broadly ref erred to as an engram. In recent years\, the term engram has been operatio nalized as an ensemble of cells that is activated by a learning experience \, undergoes plasticity\, and enables specific memory recall. Engram label ling methodologies are now opening new avenues for investigating how learn ed and innate representations are behaviourally expressed. \n\nIn this sem inar\, I will introduce the background of the broader memory engram field. I will describe how engram cell labelling methodologies allow us to genet ically label\, observe\, and manipulate the specific ensembles of neurons that encode particular memories in the rodent brain. I will then describe our recent research on innate and acquired forms or long-term forgetting i n the mouse\, by focussing on natural forgetting in adults and infantile a mnesia during development. I will outline a novel framework that considers both natural and pathological forgetting to be predictive processes that involve the interaction of a subject's priors with perceptual experience. I will introduce a perspective whereby instincts can be conceived as innat ely constructed ensembles that can functionally interact with memory engra ms. Finally\, I will describe our recent research into how engrams formed under thermal challenges can influence brain-body interactions to regulate whole body metabolism.\nSpeakers:\nAssociate Professor Tomás Ryan (Trini ty College Dublin) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/ea710d9d-7005-4414-8776-ce171b8fc38a/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Engrams as a substrate for information storage - Associat e Professor Tomás Ryan (Trinity College Dublin) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:MRI of Brain Plasticity - Professor Alan P. Koretsky\, PhD (Nation al Institutes of Health) DTSTART;VALUE=DATE-TIME:20240917T160000 DTEND;VALUE=DATE-TIME:20240917T170000 UID:https://talks.ox.ac.uk/talks/id/77ce5625-6e62-4ced-8e14-02983c36097e/ DESCRIPTION:\nSpeakers:\nProfessor Alan P. Koretsky\, PhD (National Instit utes of Health) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/77ce5625-6e62-4ced-8e14-02983c36097e/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:MRI of Brain Plasticity - Professor Alan P. Koretsky\, Ph D (National Institutes of Health) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Glymphatic dysfunction as a driver of Alzheimer’s disease: Movin g past the hype - Professor Jeffrey Iliff (University of Washington) DTSTART;VALUE=DATE-TIME:20240911T130000 DTEND;VALUE=DATE-TIME:20240911T140000 UID:https://talks.ox.ac.uk/talks/id/2f253d72-84b2-48b4-a827-e682586db401/ DESCRIPTION:The glymphatic system was initially described in rodents twelv e years ago as a brain-wide network of perivascular pathways along which t he cerebrospinal fluid surrounding the brain exchanges with the brain’s interstitial fluid\, supporting the clearance of solutes and wastes includ ing amyloid beta and tau. Reported to be active primarily during sleep\, t his model provided a compelling explanation for the restorative effects of sleep on cognition\, and for the clinical association between aging\, bra in injury\, and sleep disruption and Alzheimer’s disease. Driven primar ily by studies in rodents whose translational relevance to human disease i s uncertain\, and buffeted by mechanistic\, technical and personal controv ersy\, belief in the central role of this biology in the pathogenesis of A lzheimer’s disease has frequently outpaced the data causally linking the m\, leading some in the field to view the science surrounding the glymphat ic system as hype and sensationalism. In this presentation\, we will clear ly define what is known about sleep-active glymphatic function\, and evalu ate the data that support the role that its dysfunction plays in the devel opment and progression of Alzheimer’s disease. We will then present emer ging data from human studies demonstrating a clear role for sleep-active g lymphatic function in the clearance of amyloid beta and tau from the human brain. We will conclude by discussing how these findings may provide a pa thway towards the primary prevention of Alzheimer’s disease.\nSpeakers:\ nProfessor Jeffrey Iliff (University of Washington) LOCATION:Dorothy Crowfoot Hodgkin Building (DCHB 20-026 Seminar Room 1)\, off South Parks Road OX1 3QU TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/2f253d72-84b2-48b4-a827-e682586db401/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Glymphatic dysfunction as a driver of Alzheimer’s disea se: Moving past the hype - Professor Jeffrey Iliff (University of Washingt on) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Capturing functional stem and immune cell states in early cortical development - Dr Balazs V Varga (University of Cambridge) DTSTART;VALUE=DATE-TIME:20240806T160000 DTEND;VALUE=DATE-TIME:20240806T170000 UID:https://talks.ox.ac.uk/talks/id/e453c3f0-e481-4126-be6e-77fbc0b79742/ DESCRIPTION:Generation of cortical neurons from endogenous progenitor cell s is limited to prenatal development. In the human brain the process start s in the first trimester and the new neurons integrate in the developing n euronal networks early on. Disturbance of this early developmental process is indicated to result in neuronal network dysfunction manifesting as psy chiatric conditions later in life. Studying how these processes are regula ted and what cells are involved would help us understand how new cortical neurons can be generated and how the establishment of new synaptic connect ions can be facilitated. In my talk I am going to present our findings on the regulation of self-renewing cortical neural stem cells and the capture of a novel immune cell state involved in the establishment of active syna pses between cortical neurons.\nSpeakers:\nDr Balazs V Varga (University o f Cambridge) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/e453c3f0-e481-4126-be6e-77fbc0b79742/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Capturing functional stem and immune cell states in early cortical development - Dr Balazs V Varga (University of Cambridge) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Cortical circuits underlying complex scene analysis - Associate Pr ofessor Kamal Sen (Boston University) DTSTART;VALUE=DATE-TIME:20240920T153000 DTEND;VALUE=DATE-TIME:20240920T163000 UID:https://talks.ox.ac.uk/talks/id/3b4e734a-00db-476a-b9aa-849e560fd029/ DESCRIPTION:Sensory systems have evolved impressive abilities to process c omplex natural scenes in a myriad of environments. In audition\, the brain ’s ability to seamlessly solve the cocktail party problem remains unmatc hed by machines\, despite a long history of intensive research in diverse fields\, ranging from neuroscience to machine learning. At a cocktail part y\, and other noisy scenes\, we can broadly monitor the entire acoustic sc ene to detect important cues (e.g.\, our names being called\, or the fire alarm going off)\, or selectively listen to a target sound source (e.g.\, a conversation partner). This flexible dual-mode processing ability of nor mal hearing listeners stands in sharp contrast to the extreme difficulty f aced by hearing impaired listeners\, hearing assistive devices\, and state -of-the-art speech recognition algorithms in noisy scenes. In this talk\, I will first describe neurons at the cortical level in songbirds which dis play dual-mode responses to spatially distributed natural sounds. I will t hen present a computational model\, which replicates key features of the e xperimental data and predicts a critical role of inhibitory neurons underl ying dual mode responses. Finally\, I will present recent data revealing s imilar phenomena in mouse auditory cortex and discuss our efforts to under stand the role of cortical inhibitory neurons using a combination of elect rophysiology\, optogenetics and computational modelling.\nSpeakers:\nAssoc iate Professor Kamal Sen (Boston University) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/3b4e734a-00db-476a-b9aa-849e560fd029/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Cortical circuits underlying complex scene analysis - Ass ociate Professor Kamal Sen (Boston University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Improving temporal coding in cochlear implants: what can animal mo dels tell us? - Professor Jan Schnupp (Gerald Choa Neuroscience Institute\ , CUHK) DTSTART;VALUE=DATE-TIME:20240712T113000 DTEND;VALUE=DATE-TIME:20240712T123000 UID:https://talks.ox.ac.uk/talks/id/08167cef-bf35-4d1f-843b-57dfccb596c8/ DESCRIPTION:Cochlear implants (CIs) are remarkable prosthetic devices whic h have allowed over one million severely deaf individuals to regain suffic ient auditory perception to have conversations on the phone\, but they are not withouh their shortcomings. For example\, patients often experience d ifficulties in utilizing temporal cues for spatial hearing or pitch percep tion. The underlying causes of this temporal processing deficit may be att ributable to both biological and technological factors. However\, investig ating the exact causes of poor temporal processing in patients is challeng ing due to the confounding influence of their clinical needs on experiment al design.\n\nTo address this\, we conducted a series of studies on neonat ally deafened rats\, examining their ability to utilize interaural time di fferences (ITDs) for localizing CI stimuli. Notably\, we found that our CI rats achieved significantly better outcomes compared to human patients\, and they exhibited the same sensitivity to ITDs as small as a few tens of microseconds that is normally only seen in normally hearing individuals. S uch high sensitivity to binaural temporal cues would likely greatly improv e the ability to hear in noisy environments if it could be replicated in h uman patients.\n\nImportantly\, our research emphasizes the importance of delivering ITDs in pulse timing rather than through stimulus envelopes for effective ITD detection. We also observed that suboptimal pulse timing ca n conflict with the processing of other spatial cues\, such as interaural level differences (ILDs). The common problems seen in current human patien t populations are therefore likely due to fact that their brains have to a dapt to inadequacies in the technology in current clinical use. Based on o ur results\, we predict that implementing improved CI processing strategie s that effectively deliver crucial temporal information in pulse timing co uld lead to significantly enhanced patient outcomes. \nSpeakers:\nProfesso r Jan Schnupp (Gerald Choa Neuroscience Institute\, CUHK) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/08167cef-bf35-4d1f-843b-57dfccb596c8/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Improving temporal coding in cochlear implants: what can animal models tell us? - Professor Jan Schnupp (Gerald Choa Neuroscience I nstitute\, CUHK) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Competitive vasodynamics in cortex and what it informs us about ne uronal activity - Professor David Kleinfeld (UC San Diego) DTSTART;VALUE=DATE-TIME:20240617T110000 DTEND;VALUE=DATE-TIME:20240617T120000 UID:https://talks.ox.ac.uk/talks/id/ce216042-baf7-4217-982f-54f6aa6f85f5/ DESCRIPTION:TBC\nSpeakers:\nProfessor David Kleinfeld (UC San Diego) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/ce216042-baf7-4217-982f-54f6aa6f85f5/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Competitive vasodynamics in cortex and what it informs us about neuronal activity - Professor David Kleinfeld (UC San Diego) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Hearing the needle in the haystack - The neural representation of vocalizations in textural noise in the auditory cortex of mice - Dr Bernha rd Englitz (Radboud University) DTSTART;VALUE=DATE-TIME:20240605T113000 DTEND;VALUE=DATE-TIME:20240605T123000 UID:https://talks.ox.ac.uk/talks/id/859c89e8-2183-452c-a43d-a737766199cf/ DESCRIPTION:Sound detection amidst noise presents an important challenge i n audition. Many naturally occurring sounds (rain\, wind) can be described and predicted statistically\, so-called sound textures. Previous research has demonstrated humans' ability to leverage this statistical predictabil ity for sound recognition\, but the neural mechanisms remain elusive. We t rained mice to detect vocalizations embedded in sound textures with differ ent statistical predictability\, while recording and optogenetically modul ating the neural activity in the auditory cortex. Mice showed improved per formance and neural representation if they sampled the statistics longer p er trial. Textures with more exploitable structure\, specifically higher c ross-frequency correlations (CFCs) improved performance\, background repre sentation and vocalization decoding. Activating parvalbumin-positive (PV) interneurons had an asymmetric effect\, improving detection and neural rep resentation of vocalizations for low\, and vice versa for high CFCs. Thus\ , mice can exploit stimulus statistics to improve the sound detection in n oise\, reflected in performance and neural activity\, while relying on PV interneurons.\nSpeakers:\nDr Bernhard Englitz (Radboud University) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/859c89e8-2183-452c-a43d-a737766199cf/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Hearing the needle in the haystack - The neural represent ation of vocalizations in textural noise in the auditory cortex of mice - Dr Bernhard Englitz (Radboud University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Polygenic Regulation of Cortical Circuit Development in Neurodevel opmental Disorders: Insights from a “Model” Copy Number Variant - Anth ony-S. LaMantia (Virginia Tech) DTSTART;VALUE=DATE-TIME:20240703T160000 DTEND;VALUE=DATE-TIME:20240703T170000 UID:https://talks.ox.ac.uk/talks/id/1e1bd1bf-fd4a-4a55-b18d-89faae7d1317/ DESCRIPTION:TBC\nSpeakers:\nAnthony-S. LaMantia (Virginia Tech) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/1e1bd1bf-fd4a-4a55-b18d-89faae7d1317/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Polygenic Regulation of Cortical Circuit Development in N eurodevelopmental Disorders: Insights from a “Model” Copy Number Varia nt - Anthony-S. LaMantia (Virginia Tech) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Towards Human Systems Biology of Sleep/Wake Cycle: The roles of Ca lcium and Phosphorylation Hypothesis of Sleep - Professor Hiroki Ueda (Sch ool of Medicine\, University of Tokyo and RIKEN Center for Biosystems Dyna mics Research (BDR)) DTSTART;VALUE=DATE-TIME:20240617T160000 DTEND;VALUE=DATE-TIME:20240617T170000 UID:https://talks.ox.ac.uk/talks/id/41ba7ef7-3721-44fb-84a0-cb3029bfb5bf/ DESCRIPTION:The field of human biology confronts three major technological hurdles: the causation problem\, complexity problem\, and heterogeneity p roblem. To overcome these challenges\, we've developed innovative approach es:\n\nMammalian next-generation genetics: Triple CRISPR for knockout (KO) mice and ES mice for knock-in (KI) mice enable causation studies without traditional breeding methods.　Whole-body/brain cell profiling techniques : CUBIC allows comprehensive cell atlas construction to unravel cellular c omposition complexity.　Accurate and user-friendly technologies for measu ring sleep and awake states: ACCEL facilitates real-world monitoring of fu ndamental brain states\, addressing human heterogeneity.\n\nIntegration of these technologies has led to significant progress in sleep research\, pa rticularly in understanding sleep regulation mechanisms and sleep function s. We've proposed the phosphorylation hypothesis of sleep\, emphasizing th e role of CaMKIIα/CaMKIIβ and calcium signaling pathways in inducing and sustaining sleep. Our studies also identified wake-promoting kinases and sleep-promoting phosphatase. Additionally\, computational studies supporte d the Wake-Inhibition-Sleep-Enhancement (WISE) hypothesis\, suggesting wak efulness inhibits synaptic efficacy while sleep enhances it.\n\nDuring the talk\, we'll discuss our findings on muscarinic acetylcholine receptors ( Chrm1 and Chrm3) as essential genes for REM sleep and their implications f or psychiatric\, neurodevelopmental\, and neurodegenerative disorders. We will discuss new insights into psychiatric disorders\, neurodevelopmental disorders\, and neurodegenerative disorders derived from the phosphorylati on hypothesis of sleep.\n\n\nReferences:\n1.Tatsuki et al. Neuron\, 90(1) : 70–85 (2016). 2. Sunagawa et al\, Cell Reports\, 14(3):662-77 (2016). 3. Susaki et al. Cell\, 157(3): 726–39\, (2014). 4. Tainaka et al. Cell\ , 159(6):911-24(2014). 5. Susaki et al. Nature Protocols\, 10(11):1709-27( 2015). 6. Susaki and Ueda. Cell Chemical Biology\, 23(1):137-57 (2016). 7. Tainaka et al. Ann. Rev. of Cell and Devel. Biol. 32: 713-741 (2016). 8. Ode et al. Mol. Cell\, 65\, 176–190 (2017). 9. Tatsuki et al\, Neurosci. Res. 118\, 48-55 (2017). 10.Ode et al\, Curr. Opin. Neurobiol. 44\, 212-2 21 (2017). 11. Susaki et al\, NPJ. Syst. Biol. Appl. 3\, 15 (2017). 12. Sh inohara et al\, Mol. Cell 67\, 783-798 (2017). 13. Ukai et al\, Nat. Proto c. 12\, 2513-2530 (2017). 14. Shi and Ueda.BioEssays 40\, 1700105 (2018). 15. Yoshida et al\, PNAS 115\, E9459-E9468 (2018). 16. Niwa et al\, Cell r eport\, 24\, 2231-2247. e7 (2018). 17. Ode and Ueda\, Front. Psychol. 11\, 575328 (2020). 18. Katori et al\, PNAS 119\, e2116729119 (2022). 19. Ode K.L. et al\, iScience 25\, 103727 (2022)\, 20. Tone D. et al\, PLOS Biolog y 2022.\n\nSPEAKER BIOGRAPHY\n\nHiroki R. Ueda is a professor at the Gradu ate School of Medicine\, The University of Tokyo. He obtained his Bachelor 's degree from the Faculty of Medicine at the University of Tokyo in 2000\ , and in 2004\, he completed his Ph.D. at the same institution. In 2003\, he was appointed as a team leader at RIKEN. Subsequently\, in 2013\, he as sumed the position of full professor at the Graduate School of Medicine\, The University of Tokyo. In 2016\, Ueda made a groundbreaking discovery by identifying the sleep-promoting kinases\, CaMKIIalpha and CaMKIIbeta. Thi s finding led him to propose the phosphorylation hypothesis of sleep\, whi ch suggests that the phosphorylation-dependent regulation of the Ca2+-depe ndent hyperpolarization pathway underlies the regulation of sleep homeosta sis in mammals. Furthermore\, in 2018\, he made another significant breakt hrough by identifying the first essential genes of REM sleep\, specificall y muscarinic receptors M1 and M3. To further expedite his research endeavo rs\, Ueda has pioneered innovative methods such as whole-brain and whole-b ody clearing and imaging techniques known as CUBIC. Additionally\, he has contributed to the field of genetics by inventing next-generation mammalia n genetic tools\, including Triple-CRISPR and ES-mice methods. These advan cements enable the streamlined production and analysis of knockout (KO) an d knock-in (KI) mice without the need for traditional crossing methods.\n\ nSpeakers:\nProfessor Hiroki Ueda (School of Medicine\, University of Toky o and RIKEN Center for Biosystems Dynamics Research (BDR)) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/41ba7ef7-3721-44fb-84a0-cb3029bfb5bf/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Towards Human Systems Biology of Sleep/Wake Cycle: The ro les of Calcium and Phosphorylation Hypothesis of Sleep - Professor Hiroki Ueda (School of Medicine\, University of Tokyo and RIKEN Center for Biosys tems Dynamics Research (BDR)) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Cell type evolution in the primate brain - Alex Pollen\, PhD (Univ ersity of California) DTSTART;VALUE=DATE-TIME:20240423T160000 DTEND;VALUE=DATE-TIME:20240423T170000 UID:https://talks.ox.ac.uk/talks/id/23da2583-2897-4cae-bb5e-7616a0948b1d/ DESCRIPTION:Primate brains vary in size and organization\, but the genetic \, developmental\, and cellular basis for these differences has been diffi cult to study due to limited experimental models. In this talk\, I will de scribe three complementary approaches for studying human-specific gene net work evolution in conserved cell types using stem cell derived models and genome engineering. Ultimately\, functional studies in great ape stem cell models\, complemented by comparisons and validation in available primary tissue\, could be applied beyond studies of progenitor cell evolution to d ecode the genetic and developmental origin of recent changes in cellular o rganization\, connectivity patterns\, myelination\, and synaptic activity that have been implicated in human cognition.\nSpeakers:\nAlex Pollen\, Ph D (University of California) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/23da2583-2897-4cae-bb5e-7616a0948b1d/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Cell type evolution in the primate brain - Alex Pollen\, PhD (University of California) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Transformation of sound representations in the auditory system acr oss wakefulness\, sleep and anesthesia - Brice Bathellier (Institut de l ’Audition\, Paris) DTSTART;VALUE=DATE-TIME:20240529T140000 DTEND;VALUE=DATE-TIME:20240529T150000 UID:https://talks.ox.ac.uk/talks/id/c2a03aa8-555a-4070-a2eb-2ea096c69f46/ DESCRIPTION:How the brain transforms information from the complex acoustic waves of natural sounds into the sound perceptions that we experience is still a mystery. We have systematically sampled the neural representations of sounds across the auditory system and identified key transformations o f the information which we think are necessary to build identifiable audit ory objects that can be associated to behavioral responses. This exquisite processing of sound information is profoundly disrupted by anesthesia\, a s early as in the first relay of the auditory system but remains intact in sleep up to the auditory cortex\, the most central structure dedicated to sound processing. Thus\, contrary to what is still often assumed\, sleep permits the detailed recognition of sounds. These results also highlight t he profound difference in perceptual awareness states produced by sleep an d anesthesia. In this talk\, I will also highlight a novel acousto-optic t echnology for ultrafast all optical imaging.\nSpeakers:\nBrice Bathellier (Institut de l’Audition\, Paris) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/c2a03aa8-555a-4070-a2eb-2ea096c69f46/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Transformation of sound representations in the auditory s ystem across wakefulness\, sleep and anesthesia - Brice Bathellier (Instit ut de l’Audition\, Paris) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Adolescent experience and a putative sensitive period for learning and decision making in mice - Professor Linda Wilbrecht (University of Ca lifornia) DTSTART;VALUE=DATE-TIME:20240508T110000 DTEND;VALUE=DATE-TIME:20240508T120000 UID:https://talks.ox.ac.uk/talks/id/724a8c46-a174-485f-b120-31ec6dde5645/ DESCRIPTION:There is growing interest in the concept of an ‘adolescent s ensitive period\,’ but this phrase can mean many things. This concept ca n be explored in laboratory mice by manipulating experience during develop ment and testing behavioral or brain function in adulthood. Another approa ch is to compare adolescent versus adult learning and brain function to lo ok for adolescent gain of function. In my talk\, I will share what we have learned using both approaches. I then hope to engage the audience in disc ussion of the idea that an adolescent sensitive period may exist in rodent s for learning and decision making (and fronto-basal ganglia circuit funct ion) to support adaptive foraging behavior (Lin et al.\, 2020\;2022).\nSpe akers:\nProfessor Linda Wilbrecht (University of California) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/724a8c46-a174-485f-b120-31ec6dde5645/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Adolescent experience and a putative sensitive period for learning and decision making in mice - Professor Linda Wilbrecht (Univers ity of California) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Cortical Circuits For Learning and Behavior: Themes and Variation - Professor Jerry Chen (Boston University) DTSTART;VALUE=DATE-TIME:20240326T110000Z DTEND;VALUE=DATE-TIME:20240326T120000Z UID:https://talks.ox.ac.uk/talks/id/32591555-fd11-4e1d-81ea-0fd4cce8dfd9/ DESCRIPTION:In the mammalian brain\, learning and behavior are carried out by cortical circuits composed of diverse neuronal cell types. The distinc t gene expression patterns of cell types define their role in the circuit. Determining how cell types are organized into cortical circuit motifs pro vides an understanding for how neural computations are implemented to give rise to learning and behavior. By extension\, genetic variation across an animal population can potentially alter cell type properties. These funct ional differences may result in individual variability in learning and beh avior. My research program seeks to identify common principles of cortica l circuit function and how they vary across individuals. I will present re cently developed vertically-integrated methods that enable simultaneous be havioral\, functional\, anatomical\, and molecular measurements to be perf ormed on individual mice. I will describe the application of these methods to dissect parahippocampal circuits involved in perception and abstract s ensory learning. In addition\, I will present new efforts to survey the ge netic correlates of individual learning by performing large-scale\, automa ted task training on recombinant outbred mice. These complementary efforts will reveal how the nervous system serves as a link between our genome an d our phenome.\nSpeakers:\nProfessor Jerry Chen (Boston University) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/32591555-fd11-4e1d-81ea-0fd4cce8dfd9/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Cortical Circuits For Learning and Behavior: Themes and V ariation - Professor Jerry Chen (Boston University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY: Neuroimmune Cardiovascular Interfaces in Atherosclerosis - Sarajo Mohanta\, PhD (Ludwig-Maximilians University\, Munich) DTSTART;VALUE=DATE-TIME:20240502T150000 DTEND;VALUE=DATE-TIME:20240502T160000 UID:https://talks.ox.ac.uk/talks/id/5a613891-b3d1-4295-a57c-2dee43cb2fd5/ DESCRIPTION:Atherosclerosis is a chronic inflammatory disease of arteries caused by plaques in the inner layer of arteries. As plaques lack nerve fi bers\, the impact of neuronal control on atherosclerosis has not been cons idered before. Since the nervous system uses the adventitia\, i.e. the out er connective tissue coat of arteries\, as their major conduit to reach di stant targets\, we hypothesized that the nervous system may interact with diseased arteries via adventitial immune cells to sense and affect atheros clerosis. We identified and functionally delineated tripartite interaction s between nerves\, immune cells and diseased arteries in murine and human atherosclerosis using tissue clearing\, multiplex immunostaining\, intact aorta imaging\, virus tracing\, and single cell transcriptomics. We observ ed that atherosclerotic adventitia segments interact with the nervous syst em by stimulating axon growth adjacent to atherosclerotic plaques. Periphe ral axon terminals directly interact with immune cells and form neuroimmun e junctions. These interactions initiate a structural artery-brain circuit that directly wire diseased arteries with the brain to sense and affect a therosclerosis via dorsal root ganglia\, sympathetic ganglia and the spina l cord. Multimodal imaging and electrophysiological nerve recordings revea led activation of central and peripheral components of artery-brain circui ts in parallel to disease progression. When these interactions are disrupt ed by systemic or local sympathetic denervation in mice\, plaque-associate d immune cell aggregates in the adventitia destabilized\, plaques shrunk a nd showed a more stable phenotype. These data provide a new disease paradi gm to understand atherogenesis through multisystemic tissue interactions b etween the nervous system\, the immune system and the cardiovascular syste m. In summary\, our data demonstrated that neuroimmune cardiovascular inte ractions affect atherosclerosis progression. These studies suggest that ne uroimmune cardiovascular interfaces represent new targets using pharmaceut ical\, surgical and bioelectronic modulations before the disease including becomes life-threatening.\nSpeakers:\nSarajo Mohanta\, PhD (Ludwig-Maximi lians University\, Munich) LOCATION: Virtual (Please contact events@dpag.ox.ac.uk for Teams Link) TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/5a613891-b3d1-4295-a57c-2dee43cb2fd5/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk: Neuroimmune Cardiovascular Interfaces in Atherosclerosis - Sarajo Mohanta\, PhD (Ludwig-Maximilians University\, Munich) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Value-modulated hippocampal and cortical reactivations - Professor Min Whan Jung (Korea Advanced Institute of Science & Technology) DTSTART;VALUE=DATE-TIME:20240311T110000Z DTEND;VALUE=DATE-TIME:20240311T120000Z UID:https://talks.ox.ac.uk/talks/id/ac54212b-911a-427a-9185-85874b42a629/ DESCRIPTION:TBC\nSpeakers:\nProfessor Min Whan Jung (Korea Advanced Instit ute of Science & Technology) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/ac54212b-911a-427a-9185-85874b42a629/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Value-modulated hippocampal and cortical reactivations - Professor Min Whan Jung (Korea Advanced Institute of Science & Technology) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Seminar in Pairs: 'Maladaptive plasticity related to early movemen t restriction in rats to better understand neurodevelopmental disorders' a nd 'Early predictive biomarkers for abnormal brain development induced by fetal growth restriction' - J-Olivier Coq (CNRS/Aix-Marseille University)\ , Atsuto Onoda (Sanyo-Onoda City University\, Japan) DTSTART;VALUE=DATE-TIME:20240209T160000Z DTEND;VALUE=DATE-TIME:20240209T170000Z UID:https://talks.ox.ac.uk/talks/id/3ed239d5-c917-4b13-a4a6-6344db4eb358/ DESCRIPTION:J-Olivier Coq: 'Maladaptive plasticity related to early moveme nt restriction in rats to better understand neurodevelopmental disorders'\ n\nChildren with neurodevelopmental disorders usually exhibit gross to fin e sensorimotor impairments\, reduced physical activity and altered interac tions with people and the environment. These disorders may co-exist with h yperactivity\, cognitive deficits\, executive dysfunctions and learning im pairments. In a series of studies in rats\, we demonstrated that limited a mounts and atypical patterns of movements\, and abnormal somatosensory fee dback during early movement restriction induced in adulthood degraded post ural and locomotor abilities\, musculoskeletal histopathology including mu scle atrophy\, hyperexcitability within the sensorimotor circuitry and mal adaptive cortical plasticity. Such maladaptive plasticity led to a functio nal disorganization of the primary somatosensory and motor cortices in the absence of cortical histopathology. Early movement restriction led to ear ly deficits in the emergence of swimming\, sensorimotor reflexes and locom otor patterns and posture with toe-walking\, as well as altered spontaneou s activity and the development of pain. In addition\, restricted rats disp layed exploratory hyperactivity and impairments in object memory tasks\, a long with minor alterations in the histological features of the hippocampa l complex. Taken all together\, these results show similarities with the s ymptoms observed in children with neurodevelopmental disorders and thus\, may contribute to explain the mechanisms underlying their emergence.\n\nAt suto Onoda - 'Early predictive biomarkers for abnormal brain development i nduced by fetal growth restriction'\n\nGlobally\, the rise in children wit h neurodevelopmental disorders such as autism spectrum disorder has been a matter of increasing concern. Fetal Growth Restriction (FGR) has been ide ntified as a risk factor for neurodevelopmental disorders. However\, curre nt diagnostic technologies are inadequate for early prediction and diagnos is of brain abnormalities in FGR infants. Therefore\, the present study fo cused on identifying biomarkers for early detection of abnormal brain deve lopment caused by FGR. This research employed a novel animal model that si mulates mild\, chronic intrauterine blood flow insufficiency (Kitase et al .\, 2020). The FGR model animals exhibited low birth weight and behavioral disorders\, mirroring clinical observations. Proteomics of cerebrospinal fluid (CSF) revealed that six proteins were significantly correlated with birth weight. Out of the six proteins identified\, four - Neuroserpin\, Al pha2-macroglobulin\, OX2 membrane glycoprotein\, and Polyubiquitin-b - exh ibited chronic abnormal expression in both CSF and serum. Histopathologica l analysis has indicated that abnormal expression of the four proteins was observed in neurons\, astrocytes\, and oligodendrocytes in the cortex and hippocampus. Furthermore\, the injection of mesenchymal stem cells\, whic h proved effective in mitigating brain function abnormalities induced by F GR\, also suppressed the abnormal expression of these four proteins. Simil ar expression patterns were also observed in human serum of newborns. Thes e results suggest that these proteins could be early predictive biomarkers and surrogate markers for FGR-related brain development abnormalities.\nS peakers:\nJ-Olivier Coq (CNRS/Aix-Marseille University)\, Atsuto Onoda (Sa nyo-Onoda City University\, Japan) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/3ed239d5-c917-4b13-a4a6-6344db4eb358/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Seminar in Pairs: 'Maladaptive plasticity related to earl y movement restriction in rats to better understand neurodevelopmental dis orders' and 'Early predictive biomarkers for abnormal brain development in duced by fetal growth restriction' - J-Olivier Coq (CNRS/Aix-Marseille Uni versity)\, Atsuto Onoda (Sanyo-Onoda City University\, Japan) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Networks of emotions in sexually dimorphic stress sensitivity - Da niela Calvigioni (Karolinska Institute\, Sweden) DTSTART;VALUE=DATE-TIME:20240227T110000Z DTEND;VALUE=DATE-TIME:20240227T120000Z UID:https://talks.ox.ac.uk/talks/id/83ecb150-f014-477c-a587-151de6c58562/ DESCRIPTION:Emotional information processing is modulated by a complex int erplay of internal and external signals. A central feature in affective di sorders is the attentional bias towards stimuli of negative valence. Notab ly\, there is an increased sensitivity to stress and increased prevalence of mood disorders in women compared to men. The etiology of affective diso rders involves diverse networks\, engaging both subcortical and cortical n eural circuits\, yet a comprehensive understanding of the heterogeneity an d the distinct functional roles of these circuits in shaping emotional res ponses remains elusive.\nA subcortical pathway with a key role in negative valence extends from the lateral hypothalamic area (LHA) to the lateral h abenula (LHb)\, eliciting robust aversive responses and contributing to de pression-like states. Our research classified neurons within the LHA–LHb pathway into six glutamatergic types\, each conveying unique emotional in formation. Notably\, estrogen-sensitive (Esr1+) LHA–LHb neurons induce a version and a sex-specific sensitivity to stress\, while neuropeptide Y-ex pressing (Npy+) LHA–LHb neurons prompt arousal and rearing behavior. The persistent aversive state induced by Esr1+ LHA–LHb neurons is encoded b y the prelimbic region of the prefrontal cortex (PFC). \nBeyond the PFC\, the insular cortex (IC)\, often referred to as 'the emotional cortex'\, pl ays a pivotal role in emotional information processing. IC encodes interoc eption\, fear\, and anxiety state transitions both in mice and in humans. Performing rabies tracing of the Esr1+ LHA–LHb pathway\, we identified a population of estrogen-sensitive pyramidal neurons in the insular cortex\ , defined their connectivity\, and investigated their functional contribut ions to emotional behaviors and aversive states.\nIn summary\, our work in vestigates the crucial role of hormone-sensitive networks in emotional inf ormation processing and sexually dimorphic stress sensitivity. \nSpeakers: \nDaniela Calvigioni (Karolinska Institute\, Sweden) LOCATION:Virtual (Please contact events@dpag.ox.ac.uk for Teams Link) TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/83ecb150-f014-477c-a587-151de6c58562/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Networks of emotions in sexually dimorphic stress sensiti vity - Daniela Calvigioni (Karolinska Institute\, Sweden) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:General anesthesia decouples cortical pyramidal neurons: a recent progress - Mototaka Suzuki (University of Amsterdam) DTSTART;VALUE=DATE-TIME:20240226T130000Z DTEND;VALUE=DATE-TIME:20240226T140000Z UID:https://talks.ox.ac.uk/talks/id/48af7f18-f601-4c78-bb9e-1dede48ec9e9/ DESCRIPTION:The mystery of general anesthesia is that it specifically supp resses consciousness by disrupting feedback signaling in the brain\, even when feedforward signaling\, and basic neuronal function are left relative ly unchanged. The mechanism for such selectiveness is unknown. Here we sho w that three different anesthetics have the same disruptive influence on s ignaling along apical dendrites in cortical layer 5 pyramidal neurons in m ice. We found that optogenetic depolarization of the distal apical dendrit es caused robust spiking at the cell body under awake conditions that was blocked by anesthesia. Moreover\, we found that blocking metabotropic glut amate and cholinergic receptors had the same effect on apical dendrite dec oupling as anesthesia or inactivation of the higher-order thalamus. If fee dback signaling occurs predominantly through apical dendrites\, the cellul ar mechanism we found would explain not only how anesthesia selectively bl ocks this signaling but also why conscious perception depends on both cort ico-cortical and thalamo-cortical connectivity. Lastly\, I will briefly di scuss the next obvious questions\, newly developed tools and theories as w ell as preliminary findings.\nSpeakers:\nMototaka Suzuki (University of Am sterdam) LOCATION:Virtual (Please contact events@dpag.ox.ac.uk for Teams Link) TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/48af7f18-f601-4c78-bb9e-1dede48ec9e9/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:General anesthesia decouples cortical pyramidal neurons: a recent progress - Mototaka Suzuki (University of Amsterdam) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Neural activity in the auditory cortex of behaving\, freely-moving rats - Eli Nelken (Hebrew University\, Israel) DTSTART;VALUE=DATE-TIME:20240222T160000Z DTEND;VALUE=DATE-TIME:20240222T170000Z UID:https://talks.ox.ac.uk/talks/id/bfea64d2-58d7-43e3-b2ea-bcd067961b5e/ DESCRIPTION:We recorded neural activity in the brains of freely-moving rat s while they performed behavioral tasks for food reward. Neuronal response s to sounds depended strongly on the behavioral state: responses during be havior had more task-relevant information than responses during passive li stening. Surprisingly\, we also observed slow firing rate modulations that were task-related\, not associated with sounds\, and substantially larger than the sound-evoked responses. Modeling suggests that the large task-re lated rate modulations shape sound-driven responses during behavior. I wil l describe approaches for analyzing the fine-grained behavior of the anima ls and for deriving hypotheses about the nature of non-auditory\, task-rel ated activity.\nSpeakers:\nEli Nelken (Hebrew University\, Israel) LOCATION:Sherrington Library (Sherrington Building)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/bfea64d2-58d7-43e3-b2ea-bcd067961b5e/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Neural activity in the auditory cortex of behaving\, free ly-moving rats - Eli Nelken (Hebrew University\, Israel) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Neural circuits underlying sleep structure and functions - Profess or Antoine Adamantidis (University of Bern) DTSTART;VALUE=DATE-TIME:20240119T160000Z DTEND;VALUE=DATE-TIME:20240119T170000Z UID:https://talks.ox.ac.uk/talks/id/14a680ed-fc02-41e9-bbdd-8f23cce1f6b5/ DESCRIPTION:Brain activity during sleep classically refers to circuit-spec ific oscillations\, including slow waves\, spindles\, sharp-wave ripples o r theta\, that are nested in thalamocortical or hippocampus networks\, res pectively. However\, the activity of other neuronal circuits is strongly m odulated during sleep states. A major challenge is to determine the neural mechanisms underlying these activities and their functional implications in health and diseases. In this lecture\, I will summarise our work on the dissection of the neural circuits underlying sleep-wake control\, sleep o scillations and their relevance to brain plasticity associated with REM sl eep\, and discuss their relevance to motivated behaviours and emotional pr ocessing. \nSpeakers:\nProfessor Antoine Adamantidis (University of Bern) LOCATION:Sherrington Building (Florence Buchanan Lecture Theatre)\, off Pa rks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/14a680ed-fc02-41e9-bbdd-8f23cce1f6b5/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Neural circuits underlying sleep structure and functions - Professor Antoine Adamantidis (University of Bern) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Synaptic routing and feed-forward neuropeptide network in the thre at connectome - Assistant Professor Janos Fuzik (Karolinska Institute\, St ockholm\, Sweden) DTSTART;VALUE=DATE-TIME:20231205T123000Z DTEND;VALUE=DATE-TIME:20231205T133000Z UID:https://talks.ox.ac.uk/talks/id/58c2e36d-f8bc-4473-bf6d-53ac206777a3/ DESCRIPTION:Mental disorders account for 30% of worldwide disease burden w ith anxiety disorders being the most frequent group of psychiatric disorde rs. Compared to men\, women have twice the risk to develop anxiety disorde rs. Threat-processing and fight-or-flight networks have crucial role in th e pathophysiology of developing anxiety disorders.\nThe periaqueductal gra y matter is an evolutionary conserved key center for integrating emotional behaviors\, such as anxiety and defensive reactions. Its dorsal aspect (d PAG) is critical for processing threatful and panicogenic stimuli. The ant erior hypothalamic nucleus (AHN) is a hub of the hypothalamic defense circ uitry that responds to exposure of threats such as the proximity of predat ors. The ventromedial hypothalamus (VMH) provides strong excitatory input both to dPAG to promote freezing and to the AHN to promote escape in roden ts and induce. Interestingly\, the VMH\, the dPAG but and the inputs of th e VMH such as the medial amygdala (MeA) are highly expressing neuropeptide s and its receptors.\nHowever\, the circuit motifs\, neuronal types and sy naptic mechanisms that respond to the VMH inputs and process the threatful information are poorly understood. We probe connectivity and synaptic pla sticity with high-throughput all-optical voltage imaging and we use Voltag e-Seq to reveal the identity of protagonist neurons within the crucial cir cuit motifs. We also aim to understand the role of feed-forward neuromodul ation by investigation of excitatory and inhibitory circuit re-routing mod ulated by neuropeptides that contributes to the long-term changes in threa t-processing circuits of dPAG\, AHN and VMH. We compare male and female ne tworks in the VMH-PAG-AHN postsynaptic connectome and the synaptic plastic ity. Neuronal cell types and their connectivity are highly conserved in ma mmals and can successfully be used as targets in the treatment of mood dis orders.\nSpeakers:\nAssistant Professor Janos Fuzik (Karolinska Institute\ , Stockholm\, Sweden) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/58c2e36d-f8bc-4473-bf6d-53ac206777a3/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Synaptic routing and feed-forward neuropeptide network in the threat connectome - Assistant Professor Janos Fuzik (Karolinska Insti tute\, Stockholm\, Sweden) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Stem cell therapy for perinatal brain injuries - Dr Yoshiaki Sato (Nagoya University Hospital) DTSTART;VALUE=DATE-TIME:20231113T150000Z DTEND;VALUE=DATE-TIME:20231113T160000Z UID:https://talks.ox.ac.uk/talks/id/fefcf6a6-1ee6-4447-b7ff-252e5c3993c8/ DESCRIPTION:Despite the significant reduction in global neonatal mortality over the last 30 years\, there are still numerous intractable perinatal d iseases requiring novel therapies\, including perinatal hypoxic-ischemic e ncephalopathy (HIE). Stem cell therapy is expected to be a promising treat ment option for such diseases\, as it has several advantages\, such as the ability to replace injured cells\, regenerate on their own\, and produce growth factors that induce therapeutic effects. Moreover\, stem cells can migrate to where they are needed\, even when administered intravenously\, and respond to the situation and location.\nWe are developing novel stem c ell-based therapies for various perinatal diseases\, focusing on HIE and b ronchopulmonary dysplasia. Regarding HIE\, we have conducted basic researc h on various types of stem cells\, such as neural stem/progenitor cells\, umbilical cord blood cells\, and mesenchymal stem cells derived from vario us tissues. Among these stem cells\, we have proceeded to a clinical trial with multilineage-differentiating stress-enduring cells. \nAdditionally\, we are focusing on the treatment of neurological symptoms in the chronic phase\, such as cerebral palsy\, and are planning a clinical trial with st em cells from human exfoliated deciduous teeth (SHED)\, which have demonst rated treatment effects in the chronic phase after HIE by animal studies.\ nIn this presentation\, I will talk about basic\, translational\, and clin ical studies on HIE and the potential of stem cell therapy as a novel trea tment for perinatal brain injuries.\n\n\nSpeakers:\nDr Yoshiaki Sato (Nago ya University Hospital) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/fefcf6a6-1ee6-4447-b7ff-252e5c3993c8/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Stem cell therapy for perinatal brain injuries - Dr Yosh iaki Sato (Nagoya University Hospital) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:The organization of the molecular force sensor in cochlear hair ce lls. DTSTART;VALUE=DATE-TIME:20231006T110000 DTEND;VALUE=DATE-TIME:20231006T120000 UID:https://talks.ox.ac.uk/talks/id/8cd63679-edc5-4595-a60f-2f8808753758/ DESCRIPTION:We have examined the role of transmembrane channel-like protei n\, TMC1\, as the central component of the hair cell mechanotransducer (ME T) channel by characterizing transduction in mice harboring mutations in t he putative pore region\, TM domains 4-7. Two mutations (Tmc1 p.D528N or T mc1 p.E520Q) decreased channel conductance and two (Tmc1 p. D569N or Tmc1 p.W554L) lowered expression. All Tmc1 mutations reduced Ca2+ influx into t he hair bundle. These mutations ultimately led to hair cell apoptosis and deafness by four weeks post-natal and corroborate TMC1 as the MET channel pore. The channel complex also contains the accessory subunit\, LHFPL5. I n Lhfpl5 knockout mice\, MET currents could still be activated by hair bun dle deflections but were reduced in amplitude and sensitivity. The working range and half-saturation of the MET current were increased and gating st iffness virtually abolished\, suggesting LHFPL5 is part of the mechanical coupling between the tip-link PCDH15 and TMC1. LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/8cd63679-edc5-4595-a60f-2f8808753758/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:The organization of the molecular force sensor in cochlea r hair cells. TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:AMPK phosphorylation of FNIP1 dictates the kinetics of lysosome an d mitochondrial biogenesis - Dr Nazma Malik (Salk Institute) DTSTART;VALUE=DATE-TIME:20230803T150000 DTEND;VALUE=DATE-TIME:20230803T160000 UID:https://talks.ox.ac.uk/talks/id/3f009131-2941-4450-ae59-310395779272/ DESCRIPTION:Cells respond to mitochondrial poisons with rapid activation o f the adenosine monophosphate-activated protein kinase (AMPK)\, causing ac ute metabolic changes through phosphorylation and prolonged adaptation of metabolism through transcriptional effects. Transcription factor EB (TFEB) is a major effector of AMPK that increases expression of lysosome genes i n response to energetic stress\, but how AMPK activates TFEB remains unres olved. We demonstrate that AMPK directly phosphorylates five conserved ser ine residues in folliculin-interacting protein 1 (FNIP1)\, suppressing the function of the folliculin (FLCN)-FNIP1 complex. FNIP1 phosphorylation is required for AMPK to induce nuclear translocation of TFEB and TFEB-depend ent increases of peroxisome proliferator-activated receptor gamma coactiva tor 1-alpha (PGC1α) and estrogen-related receptor alpha (ERRα) messenger RNAs. Thus\, mitochondrial damage triggers AMPK-FNIP1-dependent nuclear t ranslocation of TFEB\, inducing sequential waves of lysosomal and mitochon drial biogenesis. \nSpeakers:\nDr Nazma Malik (Salk Institute) LOCATION:Online - email hod-pa@dpag.ox.ac.uk for the details TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/3f009131-2941-4450-ae59-310395779272/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:AMPK phosphorylation of FNIP1 dictates the kinetics of ly sosome and mitochondrial biogenesis - Dr Nazma Malik (Salk Institute) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Lessons from the deep: using electrophysiology & visualization to learn how the brain survives at sea - Dr Jessica Kendall-Bar (Center for Marine Biotechnology & Biomedicine at Scripps Institution of Oceanography\ , UC San Diego) DTSTART;VALUE=DATE-TIME:20230803T110000 DTEND;VALUE=DATE-TIME:20230803T120000 UID:https://talks.ox.ac.uk/talks/id/5843c079-16e6-4f7e-8eaf-83c52675acfb/ DESCRIPTION:Dr Kendall-Bar's interdisciplinary approach combines engineeri ng\, visualization\, and computation to learn how the brain survives at se a. This seminar will review her work to create innovative tools to detect\ , visualize\, and analyze the physiology and behavior of animals in extrem e environments that showcase their biological resilience to oxygen and sle ep deprivation. From individuals to ecosystems\, Kendall-Bar conducts mult idisciplinary physiological studies that combine basic and applied science with potential to advance conservation and translational medicine. This s eminar reviews Kendall-Bar's dissertation research on sleep in seals and p resents some current and ongoing projects to combine high-performance comp uting and visualization to assess brain activity in human freedivers\, epi lepsy in sea lions\, and cardiac performance in some of the largest (blue whales) and smallest (emperor penguins) divers.\n\nJessica Kendall-Bar wil l also share her experience creating the communications material surroundi ng her latest paper\, published in April 2023 in Science (Brain activity o f diving seals reveals short sleep cycles at depth) that was featured by t he CNN\, NPR\, BBC\, The New York Times\, The Atlantic\, The Washington Po st\, and National Geographic.\n\nSPEAKER BIOGRAPHY\n\nDr Jessica Kendall-B ar is a Schmidt AI in Science Postdoctoral Fellow at the Center for Marine Biotechnology & Biomedicine at Scripps Institution of Oceanography\, UC S an Diego. Kendall-Bar’s postdoctoral work builds on her doctoral researc h at UC Santa Cruz\, where she developed new tools to non-invasively measu re and visualize the sleep patterns of wild seals. At Scripps\, Kendall-Ba r seeks to compare the extreme physiology of elite divers- including human s\, penguins\, seals\, and whales. Kendall-Bar also believes that scientif ic progress is futile unless communicated effectively. Her animations\, il lustrated children’s books\, and data visualizations aim to accurately p ortray science and its role in preserving underwater ecosystems. Her work as a science communication specialist distills scientific complexity into data-driven stories\, graphics\, and animations that accelerate research\, outreach\, and conservation.\n\nTEAMS LINK\n\nThe lecture is viewable via : https://teams.microsoft.com/l/meetup-join/19%3ameeting_YTNmMjg5ZDUtMTQyN S00ZTVmLWE3NjItMjA0ZjkyMTg0ZDY0%40thread.v2/0?context=%7b%22Tid%22%3a%22cc 95de1b-97f5-4f93-b4ba-fe68b852cf91%22%2c%22Oid%22%3a%221f280292-0175-4318- bef1-cbb104ca0801%22%7d\nSpeakers:\nDr Jessica Kendall-Bar (Center for Mar ine Biotechnology & Biomedicine at Scripps Institution of Oceanography\, U C San Diego) LOCATION:Sherrington Library (This is a hybrid event - with the speaker at tending in-person and viewable on Teams)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/5843c079-16e6-4f7e-8eaf-83c52675acfb/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Lessons from the deep: using electrophysiology & visualiz ation to learn how the brain survives at sea - Dr Jessica Kendall-Bar (Ce nter for Marine Biotechnology & Biomedicine at Scripps Institution of Ocea nography\, UC San Diego) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Mechanism of energy intake and expenditure regulation by coding an d non-coding genes in the neurons of the melanocortin system - Ilya A. Vin nikov (Shanghai Jiaotong University) DTSTART;VALUE=DATE-TIME:20230706T140000 DTEND;VALUE=DATE-TIME:20230706T150000 UID:https://talks.ox.ac.uk/talks/id/b0708289-65ff-4e74-a836-1aa53fea88b5/ DESCRIPTION:Obesity is a worldwide growing epidemic. The arcuate nucleus o f the hypothalamus (ARC) comprises the first order neurons such as proopio melanocortin (POMC)- and agouti-related protein-expressing neurons signali ng to various extra-hypothalamic and hypothalamic cells\, such as oxytocin neurons within the paraventricular nucleus (PVH). In this presentation\, I aim to demonstrate how pharmacological in vivo reductionist approach led us to identification of microRNAs such as miR-29 critical for a proper me tabolic balance. Moreover\, in situ CRISPR-Cas9-dependent inactivation of this microRNA in POMC neurons or glucocorticoid receptor in oxytocin neuro ns resulted in hyperphagia and obesity accompanied by insulin resistance\, imbalanced fat/lean distribution as well as other metabolic changes. Impo rtantly\, identification and validation of the downstream targets allowed us to develop approaches to rescue these metabolic phenotypes.\n\nSPEAKER BIOGRAPHY\n\nAfter graduation from the Medical faculty of the Moscow State University in 2003\, Ilya A. Vinnikov has earned his doctoral degree in 2 008 at the University of Heidelberg. The following postdoc training was ob tained at the German Cancer Research Center (DKFZ) Heidelberg. Since 2016\ , he is a tenure track associate professor of the School of Life Sciences and Biotechnology at the Shanghai Jiao Tong University. The main research interests of Prof. Vinnikov’s Laboratory of Molecular Neurobiology compr ise deciphering the mechanisms of genetic\, epigenetic\, transcriptional a nd post-transcriptional regulation of biological systems and understanding their physiological relevance in the evolutionary context. His studies on diabetes mellitus\, obesity and neurodegeneration were published in Natur e Medicine\, Journal of Neuroscience\, Cell Death and Disease\, Molecular Metabolism and other journals. The lab uses in situ Cre-dependent CRISPR-C as9-based genetic approaches and other genetic\, epigenetic and pharmacolo gical tools with high cellular and molecular resolution to manipulate the genes of interest in specific cell populations of mice and nematodes. Vinn ikov’s research group was the first to demonstrate an age-related declin e of microRNAs and their critical physiological role in dopamine neurons. Moreover\, in their recent works\, they used an originally developed stabi lized microRNA mimics delivery reductionist approach to identify hypothala mic microRNAs protecting mice from obesity. The integrated solutions devel oped by Vinnikov lab to monitor and analyze metabolic and age-related para meters by implantable sensors will help translate these research findings to patients.\nSpeakers:\nIlya A. Vinnikov (Shanghai Jiaotong University) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/b0708289-65ff-4e74-a836-1aa53fea88b5/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Mechanism of energy intake and expenditure regulation by coding and non-coding genes in the neurons of the melanocortin system - Il ya A. Vinnikov (Shanghai Jiaotong University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Diabetes associated gene TCF7L2 links brain energy metabolism wit h social deficits - Marta B. Wiśniewska (Centre of New Technologies\, Uni versity of Warsaw) DTSTART;VALUE=DATE-TIME:20230522T160000 DTEND;VALUE=DATE-TIME:20230522T170000 UID:https://talks.ox.ac.uk/talks/id/4c50bfbc-a5ae-48c6-87a8-2e7b1bfcd764/ DESCRIPTION:Energy metabolism deficits are prevalent in autism spectrum di sorder (ASD) and other mental conditions\; however\, causes of this comorb idity remain a puzzle. Genetic studies strongly implicated Wnt/β-catenin signalling and its effector the TCF7L2 transcription factor in neurodevelo pmental disorders\, including ASD. On the other hand\, TCF7L2 gene variant s are the strongest risk factors for type II diabetes. In my presentation\ , I will show experimental evidence that TCF7L2\, in addition to its funct ions in the metabolic tissues\, regulates energy metabolism in the highly interconnected thalamocortical circuit. Furthermore\, thalamic deficiency of TCF7L2 causes autism-like behaviours. To explore the potential link bet ween brain energy metabolism and ASD\, we fed Tcf7l2-cKO mice with ketogen ic diet\, which normalised brain energy metabolism and improved social int eractions. We propose that ASD can originate from compromised energy metab olism in thalamocortical circuits\, and ketogenic diet may ameliorate core ASD symptoms in patients with enhanced aerobic glycolysis.\nSpeakers:\nMa rta B. Wiśniewska (Centre of New Technologies\, University of Warsaw) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/4c50bfbc-a5ae-48c6-87a8-2e7b1bfcd764/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Diabetes associated gene TCF7L2 links brain energy metab olism with social deficits - Marta B. Wiśniewska (Centre of New Technolog ies\, University of Warsaw) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Brain-wide neural circuits for sensory-guided behavior - Assistant Professor Ross Williamson (University of Pittsburgh) DTSTART;VALUE=DATE-TIME:20230619T160000 DTEND;VALUE=DATE-TIME:20230619T170000 UID:https://talks.ox.ac.uk/talks/id/f38dbcfe-5ce0-43a0-800a-7158b8cb7239/ DESCRIPTION:Auditory-guided behavior is ubiquitous in everyday life\, when ever auditory information is used to guide the decisions we make and the a ctions we take. One such behavior is auditory categorization\, a process t hat reflects the ability to transform bottom-up sensory stimuli into discr ete perceptual categories and use these perceptual categories to drive a s ubsequent action. Although this process is well-documented at the behavior al and cognitive levels\, surprisingly little is known about the explicit neural circuit mechanisms that underlie categorical computation and how th e result of this computation drives behavioral outcomes. We believe that t he transformation of auditory information into an appropriate behavioral r esponse is necessarily a brain-wide endeavor. The deep layers of the audit ory cortex give rise to several massive projection systems that exert infl uence over many downstream brain areas. Here\, I will discuss our efforts towards understanding the organization of these projection systems and how they differentially contribute to auditory-guided behavior.\nSpeakers:\nA ssistant Professor Ross Williamson (University of Pittsburgh) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/f38dbcfe-5ce0-43a0-800a-7158b8cb7239/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Brain-wide neural circuits for sensory-guided behavior - Assistant Professor Ross Williamson (University of Pittsburgh) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Thalamus drives coupling of information streams in cortical dendri tes - Dr Arco Bast (Lab of Marcel Oberlaender\, MPI for Neurobiology of Be havior\, Germany) DTSTART;VALUE=DATE-TIME:20230516T110000 DTEND;VALUE=DATE-TIME:20230516T120000 UID:https://talks.ox.ac.uk/talks/id/f6f5c187-214d-4f73-9072-4e7542422122/ DESCRIPTION:Perception is linked to a calcium-dependent spiking mechanism that is built into the distal dendrites of layer 5 pyramidal tract neurons (L5PTs) - the major output cell type of the cerebral cortex. It is yet un clear which circuits activate this cellular mechanism upon sensory stimula tion. Here we found that the same thalamocortical axons that relay sensory signals to layer 4 also densely target the dendritic domain by which pyra midal tract neurons initiate calcium spikes. Distal dendritic inputs\, whi ch normally appear greatly attenuated at the cell body\, thereby generate bursts of action potentials in cortical output upon stimulus onset. Our fi ndings indicate that thalamus drives an active dendritic mechanism to coup le sensory signals with top-down information streams into cortical output. Thus\, in addition to being the central hub for sensory signals\, thalamu s is also likely to ensure that the signals it relays to cortex are percei ved by the animal.\nSpeakers:\nDr Arco Bast (Lab of Marcel Oberlaender\, M PI for Neurobiology of Behavior\, Germany) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/f6f5c187-214d-4f73-9072-4e7542422122/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Thalamus drives coupling of information streams in cortic al dendrites - Dr Arco Bast (Lab of Marcel Oberlaender\, MPI for Neurobiol ogy of Behavior\, Germany) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Evolution and Development of Mammalian Brains - Professor Zoltan M olnar (DPAG\, University of Oxford)\, Professor Verónica Martínez-Cerde ño (Institute for Paediatric Regenerative Medicine at Shriners Hospitals for Children\, Institute for Medical Investigation of Neurodevelopmental D isorders - MIND\, School of Medicine\, University of California\, Davis)\, Professor Stephen Charles Noctor (Department of Psychiatry and Behavioura l Sciences\, UC Davis)\, Professor Chiaki Ohtaka-Maruyama (Developmental N euroscience Project\, Tokyo Metropolitan Institute of Medical Science\, To kyo\, Japan)\, Professor Paul R. Manger (School of Anatomical Sciences\, F aculty of Health Sciences\, University of the Witwatersrand\, Johannesburg \, South Africa)\, Associate Professor Rogier B. Mars (Wellcome Centre for Integrative Neuroimaging\, University of Oxford and Donders Institute for Brain\, Cognition and Behavior\, Radboud University Nijmegen)\, Jasper E. Hunt (Nuffield Department of Clinical Neurosciences\, University of Oxfor d) DTSTART;VALUE=DATE-TIME:20230626T090000 DTEND;VALUE=DATE-TIME:20230626T130000 UID:https://talks.ox.ac.uk/talks/id/19239874-73f8-4ac1-b083-e3d96b525db5/ DESCRIPTION:PROGRAMME\n\n09:00: Coffee\n\n09:15: Introduction by Professor Zoltán Molnár\n\n09:30: 'Astrocyte evolution – from vertebrates to hu man' by Professor Verónica Martínez-Cerdeño \n\n10:00: 'Intrinsic and e xtrinsic factors that impact the function of neural precursor cells in the fetal cerebral cortex under normal and pathological conditions' by Stephe n Charles Noctor\n\n10:30: 'Molecular mechanisms underlying the subplate l ayer expansion in primates during brain evolution' by Professor Chiaki Oht aka-Maruyama\n\n11:00: Coffee\n\n11:30: 'Neurothermodynamics and global ge ometry of the mammalian brain' by Professor Paul R. Manger\n\n12:00: 'A co mmon space approach to comparative neuroscience' by Associate Professor Ro gier B. Mars\n\n12:30: 'Effects of lifestyle and phylogeny on the vertebra te visual system' by Wellcome Trust DPhil Student Jasper E. Hunt\n\nABSTRA CTS\n\n'Astrocyte evolution – from vertebrates to human' by Professor Ve rónica Martínez-Cerdeño PhD\n\nTwo major types of astrocytes have been broadly described in mammals\, the protoplasmic and fibrous astrocytes. Tw o other astrocyte types with distinct morphology are known to localize to specific layers of the cerebral cortex in primates\, interlaminar astrocyt es (ILAs) and varicose-projection astrocytes (VP-As). ILAs possess a cell body in cortical layer I\, and long processes traveling perpendicular to t he pia towards deeper layers of the cortex. We examined cerebral cortex fr om 46 species that encompassed most orders of therian mammalians\, includi ng 22 primate species. Pial ILA were present in all mammalian species ana lyzed\, and that while the density of pial ILA somata only varied slightly \, the complexity of ILA processes varied greatly across species. Primates \, specifically bonobo\, chimpanzee\, orangutan\, and human\, exhibited pi al ILA with the highest complexity. We described two distinct cell types w ith interlaminar processes that have been referred to as ILA\, that we ter med pial ILA and supial ILA (Falcone et al.\, 2019). VP-As have a cell bod y in layers V-VI\, short spiny processes\, and one to five long processes with prominent\, evenly spaced varicosities. We found that VP-As were pres ent only in human and other apes (hominoids) and were absent in all other species. The presence of VP-As was concomitant with the presence of inter laminar astrocytes that also have varicosities along the interlaminar proc ess (Falcone et al.\, 2022).\n\n'Intrinsic and extrinsic factors that impa ct the function of neural precursor cells in the fetal cerebral cortex und er normal and pathological conditions' by Professor Stephen Charles Noctor \, PhD\n\nThe Noctor Lab investigates development of the cerebral cortex\, with a special focus on factors that regulate neural and glial precursor cells and the migration of cortical cells. Goals of the lab include establ ishing a firm foundation for understanding signaling systems that control normal brain development to better understand the origins of neurodevelopm ental disorders. We investigate brain development in a variety of vertebra tes\, including rodents and mammalian species that possess gyrencephalic c erebral cortex. Our current work investigates the complex milieu in cortic al proliferative zones\, and how cellular interactions regulate normal dev elopmental programs that include cell genesis and cellular migration.\n\n' Molecular mechanisms underlying the subplate layer expansion in primates d uring brain evolution' by Professor Chiaki Ohtaka-Maruyama PhD\n\nThe subp late(SP) layer of the mammalian neocortex plays an essential role in the e mbryonic cortical formation\, including establishing a thalamocortical con nection and radial neuronal migration. Primates such as monkeys and humans have a transiently highly expanded SP layer during the embryonic period c ompared to mice. However\, its biological significance and the molecular m echanisms responsible for this expansion still need to be understood. We a imed to elucidate the mechanism by performing Visium spatial transcriptomi c analysis using the embryonic cerebrum of marmosets and humans. By compar ing these data with mouse data to identify genes specifically expressed in the SP layer of the primate. I want to discuss the candidate genes identi fied in this analysis an d their functional roles in expanding the SP laye r in primates.\n\n'Neurothermodynamics and global geometry of the mammalia n brain' by Professor Paul R. Manger PhD\n\nThe mammalian brain produces h eat independently of the body\, indicating that thermodynamics specificall y the relationship between heat production and heat loss might be an impor tant factor in the evolution of global brain shape. Mammalian neurons need to be maintained at around 37 degrees C in order to function properly\, a nd this temperature requirement might be a significant factor in mammalian brain evolution. By examining the relationship between a proxy for heat p roduction in the brain (the endocranial volume) and heat loss (endocranial surface area) across over 450 mammal species\, interesting findings emerg e. For “most mammals” there is a distinct relationship between these t wo parameters indicating an ancestral balance between heat production and loss that appears to work for the spheroid shaped mammalian brain. In rode nts the brain takes on a more tubular shape than other mammals\, indicatin g the potential need to increase heat production in the brain to counter t he increased rate of heat loss. In cetaceans\, the brain takes on a more s pherical shape\, reducing surface area by around 10%\, indicating a loweri ng in the rate of heat loss. In primates\, there is a clear relationship b etween increasing brain size and increasing sphericity of the brain\, culm inating in hominins having quite spheroidal shaped brains\, with a reducti on in surface area of around 15%. Thus\, both cetaceans and larger-brained primates can reduce the energetic costs required to heat the brain\, alth ough they achieve this in different ways. Energetic savings may be quite u seful in the context of natural selection.\n\n'A common space approach to comparative neuroscience' by Associate Professor Rogier B. Mars\, PhD\n\nO ur laboratory is interested in developing a large-scale approach to compar ative neuroscience. Using neuroimaging\, we are able to get whole-brain\, multi-modal images of post-mortem specimens\, which allow us to sample an unprecedented range of species at high anatomical specificity. We have con centrated on developing approaches to quantitatitvely compare the organiza tion of mammalian brains\, even if they differ strongely in size and morph ology. In this talk I will report our recent progress.\n\n'Effects of life style and phylogeny on the vertebrate visual system' by Jasper E. Hunt\, M Sc\n\nComparing CNS development and organisation between animals has yield ed new insights into animals’ evolutionary histories\, yet the role of e cological considerations in shaping CNS evolution is relatively underexplo red. Nonetheless\, ecological considerations play a considerable role in d riving selection and thus shape evolution of the nervous system. My DPhil aims to fill this gap\, underscoring the importance of an animal’s envir onment and behavioural lifestyle for the evolution of its nervous system.\ n\nVision enables vertebrates from across the animal kingdom to interact w ith their environments\, presenting a fantastic opportunity to examine how ecological pressures have shaped these animals’ behaviours and their de velopmental strategies. To begin exploring how the environment shapes visu al system evolution\, I develop a theoretical framework wherein ethologica l considerations are used to generate testable hypotheses regarding visual system development and organisation across species.\n\nFirst\, I use this ethological framework to advance a novel interpretation of the cross-spec ies significance of retinal waves\, a well-characterised phenomenon in vis ual system development. This theoretical work has led to a new collaborati on with the Ruthazer Lab\, which will result in my theory’s predictions being tested in an understudied species.\n\nUsing the same ethological fra mework\, I develop hypotheses regarding the organisation of occipital whit e matter tracts in the primate lineage. Having validated a data-driven tra ctographic technique that is well-suited for cross-species comparisons\, I will begin to test these ethologically-motivated hypotheses regarding pri mate visual organisation.\nSpeakers:\nProfessor Zoltan Molnar (DPAG\, Univ ersity of Oxford)\, Professor Verónica Martínez-Cerdeño (Institute for Paediatric Regenerative Medicine at Shriners Hospitals for Children\, Inst itute for Medical Investigation of Neurodevelopmental Disorders - MIND\, S chool of Medicine\, University of California\, Davis)\, Professor Stephen Charles Noctor (Department of Psychiatry and Behavioural Sciences\, UC Dav is)\, Professor Chiaki Ohtaka-Maruyama (Developmental Neuroscience Project \, Tokyo Metropolitan Institute of Medical Science\, Tokyo\, Japan)\, Prof essor Paul R. Manger (School of Anatomical Sciences\, Faculty of Health Sc iences\, University of the Witwatersrand\, Johannesburg\, South Africa)\, Associate Professor Rogier B. Mars (Wellcome Centre for Integrative Neuroi maging\, University of Oxford and Donders Institute for Brain\, Cognition and Behavior\, Radboud University Nijmegen)\, Jasper E. Hunt (Nuffield Dep artment of Clinical Neurosciences\, University of Oxford) LOCATION:Sherrington Building (Sherrington Room (second floor))\, off Park s Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/19239874-73f8-4ac1-b083-e3d96b525db5/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Evolution and Development of Mammalian Brains - Professor Zoltan Molnar (DPAG\, University of Oxford)\, Professor Verónica Martín ez-Cerdeño (Institute for Paediatric Regenerative Medicine at Shriners Ho spitals for Children\, Institute for Medical Investigation of Neurodevelop mental Disorders - MIND\, School of Medicine\, University of California\, Davis)\, Professor Stephen Charles Noctor (Department of Psychiatry and Be havioural Sciences\, UC Davis)\, Professor Chiaki Ohtaka-Maruyama (Develop mental Neuroscience Project\, Tokyo Metropolitan Institute of Medical Scie nce\, Tokyo\, Japan)\, Professor Paul R. Manger (School of Anatomical Scie nces\, Faculty of Health Sciences\, University of the Witwatersrand\, Joha nnesburg\, South Africa)\, Associate Professor Rogier B. Mars (Wellcome Ce ntre for Integrative Neuroimaging\, University of Oxford and Donders Insti tute for Brain\, Cognition and Behavior\, Radboud University Nijmegen)\, J asper E. Hunt (Nuffield Department of Clinical Neurosciences\, University of Oxford) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Anatomical organization and function of oxytocin system in the mou se brain - Associate Professor Yongsoo Kim (Department of Neural and Behav ioral Sciences\, College of Medicine\, The Pennsylvania State University) DTSTART;VALUE=DATE-TIME:20230511T160000 DTEND;VALUE=DATE-TIME:20230511T170000 UID:https://talks.ox.ac.uk/talks/id/e468dab9-7d10-4551-82d3-916359e79b78/ DESCRIPTION:Oxytocin (Oxt) neurons regulate diverse physiological response s via direct connections with different neural circuits. However\, the lac k of comprehensive input-output wiring diagrams of Oxt neurons and their q uantitative relationship with Oxt receptor (Oxtr) expression presents chal lenges to understanding circuit-specific Oxt functions. In this talk\, I w ill first present my lab’s effort to understand spatiotemporal trajector ies of Oxtr expression in postnatally developing mouse brains\, anatomic c onnectivity maps of Oxt neurons\, and their relationship with Oxtr express ion. I developed and utilized high resolution mapping methods to visualize and quantify cellular resolution signals across the entire mouse brain us ing 3D reference atlases. Our detailed Oxt wiring diagram provides anatomi c insights about the distinct behavioral functions of Oxt signaling in the brain. Secondly\, I will present our ongoing effort to understand the ana tomy and function of Oxtr neurons in the dorsal endopiriform nucleus (EPd) . The EPd is a largely understudied cortical subplate area that contains a high density of Oxtr neurons. We are utilizing a combination of a cell ty pe specific Cre driver\, viral tools\, 3D mapping methods\, and in vivo ne ural activity recording to comprehensively gain novel insight of the EPd n eurons. We found strong EPd connectivity with olfactory and limbic cortice s and identified a sustained decrease in neural activity upon novel stimul i. Collectively\, our research advances neuroanatomical understanding of O xt system in the brain and how it regulates different behaviors. \nSpeaker s:\nAssociate Professor Yongsoo Kim (Department of Neural and Behavioral S ciences\, College of Medicine\, The Pennsylvania State University) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/e468dab9-7d10-4551-82d3-916359e79b78/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Anatomical organization and function of oxytocin system i n the mouse brain - Associate Professor Yongsoo Kim (Department of Neural and Behavioral Sciences\, College of Medicine\, The Pennsylvania State Uni versity) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Thalamocortical neuron firing and spindle oscillations driven by t halamus-specific transcription factor\, Shox2 - Dr Isabella Febbo (Tulane University) DTSTART;VALUE=DATE-TIME:20230306T110000Z DTEND;VALUE=DATE-TIME:20230306T120000Z UID:https://talks.ox.ac.uk/talks/id/486d3a08-ab15-452c-adf6-215e1560e7d3/ DESCRIPTION:\nSpeakers:\nDr Isabella Febbo (Tulane University) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/486d3a08-ab15-452c-adf6-215e1560e7d3/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Thalamocortical neuron firing and spindle oscillations dr iven by thalamus-specific transcription factor\, Shox2 - Dr Isabella Febbo (Tulane University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Calcium and metabolic activity in cortical astrocytes during locom otion in mice - Professor Alexey Semyanov (Jiaxing University College of M edicine\, China) DTSTART;VALUE=DATE-TIME:20230224T160000Z DTEND;VALUE=DATE-TIME:20230224T170000Z UID:https://talks.ox.ac.uk/talks/id/896c609d-4d4d-4d6a-a738-899e4d356990/ DESCRIPTION:The brain active milieu concept holds that the brain function depends on interactions among neurons\, glial cells\, cells of blood vesse ls\, extracellular space\, and extracellular matrix. Within this framework \, we investigate the function of astrocytes that form networks and intera ct with all other elements of the brain active milieu. Astrocytes are not electrically excitable cells but can generate complex spatiotemporal patte rns of calcium activity. We investigated different parameters of these pat terns recorded in cortical astrocytes with two-photon calcium imaging in a wake mice moving on a rotating platform. We also studied calcium activity in hippocampal astrocytes using fibre photometry. In a quiescent state of the animal\, calcium activity was characterized by small but regular fluct uations. During running episodes\, astrocytic calcium increased significan tly in spread and amplitude. Such calcium elevations had a latency from th e running onsets and outlasted the running episodes. The functional releva nce of delayed and slow calcium transients in the astrocytic network is cu rrently unclear. It could be associated with memory storage or metabolic p rocesses. Therefore\, we performed label-free metabolic imaging (Raman mic rospectrometry) in awake mice running on a treadmill. We observed that run ning episodes correlate with prolonged increases in the amount of reduced mitochondrial cytochromes in astrocytes but not neurons. On the contrary\, the amount of reduced cytochromes in neurons decreased. Our results demon strate the strong involvement of cortical astrocytes in the brain activity associated with animal behaviour. \nSpeakers:\nProfessor Alexey Semyanov (Jiaxing University College of Medicine\, China) LOCATION:Sherrington Building (Sherrington Room (second floor))\, off Park s Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/896c609d-4d4d-4d6a-a738-899e4d356990/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Calcium and metabolic activity in cortical astrocytes dur ing locomotion in mice - Professor Alexey Semyanov (Jiaxing University Col lege of Medicine\, China) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:A cell-type specific brain circuit for curiosity - Dr Mehran Ahmad lou (University College London) DTSTART;VALUE=DATE-TIME:20230207T143000Z DTEND;VALUE=DATE-TIME:20230207T153000Z UID:https://talks.ox.ac.uk/talks/id/8c8860c6-8bb9-4980-ab5b-3f71231a0219/ DESCRIPTION:Motivational drives are internal states that can be different even in similar interactions with external stimuli. Curiosity as the motiv ational drive for novelty-seeking and investigating the surrounding enviro nment is for survival as essential and intrinsic as hunger. Curiosity\, hu nger\, and appetitive aggression drive three different goal-directed behav iors—novelty seeking\, food eating\, and hunting— but these behaviors are composed of similar actions in animals. This similarity of actions has made it challenging to study novelty seeking and distinguish it from eati ng and hunting in non-articulating animals. The brain mechanisms underlyin g this basic survival drive\, curiosity\, and novelty-seeking behavior hav e remained unclear. In spite of having well-developed techniques to study mouse brain circuits\, there are many controversial and different results in the field of motivational behavior. This has left the functions of moti vational brain regions such as the zona incerta (ZI) still uncertain. Not having a transparent\, nonreinforced\, and easily replicable paradigm is o ne of the main causes of this uncertainty. Therefore\, we chose a simple s olution to conduct our research: giving the mouse freedom to choose what i t wants—double free-access choice. By examining mice in an experimental battery of object free-access double-choice (FADC) and social interaction tests—using optogenetics\, chemogenetics\, calcium fiber photometry\, mu ltichannel recording electrophysiology\, and multicolor mRNA in situ hybri dization—we uncovered a cell type–specific cortico-subcortical brain c ircuit of the curiosity and novelty-seeking behavior. We found in mice tha t inhibitory neurons in the medial ZI (ZIm) are essential for the decision to investigate an object or a conspecific. These neurons receive excitato ry input from the prelimbic cortex to signal the initiation of exploration . This signal is modulated in the ZIm by the level of investigatory motiva tion. Increased activity in the ZIm instigates deep investigative action b y inhibiting the periaqueductal gray region. A subpopulation of inhibitory ZIm neurons expressing tachykinin 1 (TAC1) modulates the investigatory be havior.\nSpeakers:\nDr Mehran Ahmadlou (University College London) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/8c8860c6-8bb9-4980-ab5b-3f71231a0219/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:A cell-type specific brain circuit for curiosity - Dr Meh ran Ahmadlou (University College London) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Glutamatergic circuits regulate gut motility - Dr Ryan Hamnett\, P hD (Kaltschmidt Lab\, Department of Neurosurgery\, Stanford University) DTSTART;VALUE=DATE-TIME:20230131T163000Z DTEND;VALUE=DATE-TIME:20230131T173000Z UID:https://talks.ox.ac.uk/talks/id/eebf97a0-5220-43de-80c0-b3d50f17c5e6/ DESCRIPTION:The enteric nervous system (ENS) is situated in the intestinal wall and autonomously controls most aspects of digestion\, including inte stinal motility. The current model of neuronal control of intestinal motil ity describes reflex circuits responding to locally detected luminal conte nts\, but provides no explanation for long-distance communication and orga n-wide responses to stimuli. However\, like the central nervous system\, t he ENS contains a diverse array of neuronal subtypes\, and the contributio ns of many of these subtypes to intestinal function are unknown. The excit atory neurotransmitter glutamate is expressed in a small number of enteric neuron subtypes\, the characteristics\, circuitry and function of which h ave been little explored. Dysregulation of glutamatergic signalling is tho ught to be involved in several pathologies of the digestive tract\, includ ing irritable bowel syndrome and ischemia/reperfusion injury. We use optog enetic activation\, immunohistochemistry and single neuron tracing of glut amatergic neurons to demonstrate their role in colonic motility. Additiona lly\, we identify a novel neuron subpopulation that expresses glutamate an d is present only in the colon. This is the first illustration of glutamat ergic neuron function in the gut\, and could represent a mechanistic basis for long-distance communication in the ENS.\nSpeakers:\nDr Ryan Hamnett\, PhD (Kaltschmidt Lab\, Department of Neurosurgery\, Stanford University) LOCATION:Microsoft Teams - join via https://tinyurl.com/3svjss5p TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/eebf97a0-5220-43de-80c0-b3d50f17c5e6/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Glutamatergic circuits regulate gut motility - Dr Ryan Ha mnett\, PhD (Kaltschmidt Lab\, Department of Neurosurgery\, Stanford Unive rsity) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Cortical ensemble dynamics encode and select hunting action sequen ces - Dr Dahee Jang (Korea Advanced Institute of Science & Technology) DTSTART;VALUE=DATE-TIME:20230208T103000Z DTEND;VALUE=DATE-TIME:20230208T113000Z UID:https://talks.ox.ac.uk/talks/id/efa7f54c-ce11-4c83-a247-895dc8a2f3c0/ DESCRIPTION:\nSpeakers:\nDr Dahee Jang (Korea Advanced Institute of Scienc e & Technology) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/efa7f54c-ce11-4c83-a247-895dc8a2f3c0/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Cortical ensemble dynamics encode and select hunting acti on sequences - Dr Dahee Jang (Korea Advanced Institute of Science & Techno logy) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:The neural basis of the stereo contrast paradox - Dr Laura Palmier i (Newcastle University) DTSTART;VALUE=DATE-TIME:20230124T110000Z DTEND;VALUE=DATE-TIME:20230124T120000Z UID:https://talks.ox.ac.uk/talks/id/5913062d-d5f2-4142-a60e-ff02cb555cb7/ DESCRIPTION:\nSpeakers:\nDr Laura Palmieri (Newcastle University) LOCATION:Sherrington Building (Florence Buchanan Lecture Theatre (second f loor))\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/5913062d-d5f2-4142-a60e-ff02cb555cb7/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:The neural basis of the stereo contrast paradox - Dr Laur a Palmieri (Newcastle University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:The Coding of Visceral Senses in the Brain - Dr Chen Ran (Stephen Liberles Laboratory\, Harvard Medical School and Howard Hughes Medical Ins titute) DTSTART;VALUE=DATE-TIME:20230125T160000Z DTEND;VALUE=DATE-TIME:20230125T170000Z UID:https://talks.ox.ac.uk/talks/id/7829521a-8f1e-4344-aa13-188f51d72e31/ DESCRIPTION:The discoveries of coding principles of vision\, olfaction\, g ustation\, audition\, and somatosensation are all landmark achievements. H owever\, principles defining how the brain processes signals from visceral organs to generate internal senses remain largely unknown. We developed a novel brainstem calcium imaging platform. Using this system\, we report t hat the brainstem uses discrete neuronal populations to encode different o rgans and combinatorial codes for different mechano- and chemosensory moda lities in the same organ. Furthermore\, organs are topographically mapped in the brainstem\, forming a “visceral homunculus”. The spatial map in the brain arises from distributed representations in the sensory ganglia and depends on local inhibition. This publication provides the first analy sis of the logic used by the brain to process interoceptive inputs. In add ition\, our study helps define the wide-open field of viscerosensory codin g\, laying the foundation for future work to comprehend the neural process ing of bodily signals throughout the brain.\nSpeakers:\nDr Chen Ran (Steph en Liberles Laboratory\, Harvard Medical School and Howard Hughes Medical Institute) LOCATION:Microsoft Teams - tinyurl.com/2da8x4yf TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/7829521a-8f1e-4344-aa13-188f51d72e31/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:The Coding of Visceral Senses in the Brain - Dr Chen Ran (Stephen Liberles Laboratory\, Harvard Medical School and Howard Hughes Me dical Institute) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:AI-driven modelling for rapid and robust cortex-wide credit assign ment - Dr Rui Ponte Costa (Faculty of Engineering & Bristol Neuroscience\, University of Bristol) DTSTART;VALUE=DATE-TIME:20221205T143000Z DTEND;VALUE=DATE-TIME:20221205T153000Z UID:https://talks.ox.ac.uk/talks/id/3b6e166b-d024-4781-8e5e-35ea2915497e/ DESCRIPTION:ABSTRACT\n\nLearning requires the brain to assign credit to bi llions of synapses. How the brain achieves this feat is one of the unsolve d mysteries in neuroscience. Recently\, inspired by deep learning\, we hav e introduced a novel model of hierarchical credit assignment in cortico-co rtical networks. Our model combines synaptic\, sub-cellular\, cellular\, m icrocircuit and cortico-cortical computations to enable error-driven learn ing of challenging tasks. I will show that in contrast to previous work ou r model (i) is consistent with experimental observations\, (ii) provides r apid credit assignment across multiple cortical areas and (iii) does not require a multi-phase learning process.\n\nExperimental evidence suggests that neuromodulation also plays a key role in controlling learning. Inspir e by deep learning we model cholinergic neuromodulation as an adaptive lea rning system. In our model cholinergic neuromodulation democratizes learni ng by continuously shifting learning to different neuronal populations. I will show that such distributed learning has two key consequences: (i) gre atly speeds up learning and (ii) produces a more distributed task-encoding . Importantly\, more distributed representations result in networks that a re more robust to perturbations (e.g. cell death)\, thereby providing the first theoretical explanation of why Cholinergic deficits are commonly ass ociated with dementia\, aging and injury.\nIn summary\, our AI-driven mode lling is opening the window to a new understanding of learning in the brai n with important implications for health and disease.\n\nSPEAKER BIOGRAPHY \n\nRui leads the Neural & Machine Learning group at the University of Bri stol. The group builds biologically-constrained AI-driven models to transf orm our understanding of how the brain learns. The group is funded by the EPSRC\, BBSRC\, Wellcome Trust\, MRC and a recently awarded ERC grant to p ursue this research program. Before starting his group Rui did postdoctora l research in computational neuroscience & machine learning at the Univ ersity of Oxford and briefly at the University of Bern. ​Previously\, he completed his PhD in 2015 at the University of Edinburgh (UK) as part of the Institute for Adaptive and Neural Computation with Mark van Rossum and P. Jesper Sjöström (funded by a FCT PhD grant). During that time Rui was also a visiting PhD student at University College London (UK) and McG ill University (Canada). Before that Rui studied computer science at the U niversity of Coimbra (Portugal). Rui used to organise the Oxford NeuroTheo ry Forum (2014-2017).\nSpeakers:\nDr Rui Ponte Costa (Faculty of Engineeri ng & Bristol Neuroscience\, University of Bristol) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/3b6e166b-d024-4781-8e5e-35ea2915497e/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:AI-driven modelling for rapid and robust cortex-wide cred it assignment - Dr Rui Ponte Costa (Faculty of Engineering & Bristol Neuro science\, University of Bristol) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Acoustic context: relevant or not\, if predictable\, we code it - Dr Livia de Hoz (Charité - Universitätsmedizin Berlin) DTSTART;VALUE=DATE-TIME:20221104T110000Z DTEND;VALUE=DATE-TIME:20221104T120000Z UID:https://talks.ox.ac.uk/talks/id/f4fccd79-5542-443a-b5ad-612bafee453a/ DESCRIPTION:Acoustic contexts - the sounds that characterize a space or an event- are rich in information. Our auditory systems readily detect and l earn the acoustic context\, often implicitly\, and use it to build expecta tions that facilitate change detection\, or background suppression. We kno w little about where and how in the brain this learning takes place. Using neuronal activity recorded from subcortical and cortical stations in the auditory system of mice exposed to predictable and unpredictable sound con texts\, I will illustrate how sensitive the auditory system is to predicta bility in the surrounding acoustic context\, whether this has the form of a passive sound stream or an interactive environment.\nSpeakers:\nDr Livia de Hoz (Charité - Universitätsmedizin Berlin) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/f4fccd79-5542-443a-b5ad-612bafee453a/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Acoustic context: relevant or not\, if predictable\, we c ode it - Dr Livia de Hoz (Charité - Universitätsmedizin Berlin) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Small molecules that restore GABAergic function as a potential the rapeutics to treat Autism Spectrum Disorder - Associate Professor James P Clement Chelliah\, PhD (Neuroscience Unit\, Jawaharlal Nehru Centre for Ad vanced Scientific Research\, Bangalore\, India) DTSTART;VALUE=DATE-TIME:20221124T160000Z DTEND;VALUE=DATE-TIME:20221124T170000Z UID:https://talks.ox.ac.uk/talks/id/84a996d7-2d8c-43c4-87a6-c842445d3838/ DESCRIPTION:A cardinal feature of human brain development is that sensory\ , cognitive\, and emotional experiences shape synapses and neural-circuit development. Neuronal activity triggers changes at the synapse\, altering the composition\, shape and strength of the synapse. These neuronal activi ty-dependent modifications are necessary for learning and memory and vario us behavioural responses\, particularly during development. These features are altered in Intellectual Disability (ID) and Autism Spectrum Disorder (ASD)\, which affects ~1% of the world’s population. Heterozygous mutati ons in SYNGAP1 are one of the primary causes of Intellectual Disability (I D) and Autism Spectrum disorder (ASD). Thereby\, aberrant maturation of de ndritic spines leads to an anomalous Excitation-Inhibition (E/I) balance a t the critical period of development. In part\, such changes are linked w ith altered chloride co-transporters\, NKCC1 and KCC2\, in animal models of Fragile-X and Rett syndrome but unknown in Syngap1+/- during different developmental stages. We show that the expression\, and function of chlori de co-transporters NKCC1 and KCC2 at P14-15 heterozygous mice is altered. In addition\, we discovered that administration of a novel GSK-3β inhibit or\, 6BIO\, during critical period of development and in the young adolesc ent rescued E/I balance and the deficits of synaptic transmission and beha vioural performance like social novelty\, anxiety and spatial memory in Sy ngap1+/- mice. Here\, we demonstrated that the GABAergic circuit was disru pted during development and modulating this circuit restored cognitive\, e motional\, and social symptoms that result from hard-wired neuronal circui t damage during development by late pharmacological intervention in adulth ood. \n\nSPEAKER BIOGRAPHY\n\nJames’ career in neuroscience started as a Research Assistant in Prof Upinder Bhalla’s laboratory. He did his PhD in Prof. Randall’s lab\, and Prof. Graham Collingridge as co-PI\, for Ph D in neuroscience at the University of Bristol\, UK\, where he worked on G roup I mGluRs’ role in synaptic and intrinsic plasticity in the hippocam pus. He moved to Scripps Research Institute\, Florida\, for a post-doc in Dr Gavin Rumbaugh’s laboratory\, along with collaborators\, did pioneeri ng work in Syngap1+/- led to the understanding of the importance of the cr itical period of neuronal development and its link to Intellectual Disabil ity (ID) and autism spectrum disorder (ASD). Since July 2013\, his lab\, u sing electrophysiology (mainly)\, 2-photon imaging\, and molecular and bio chemical techniques\, continues to study how mutations in genes encoding p roteins necessary for synaptic function cause ID and ASD using Syngap1+/- the Jawaharlal Nehru Centre for Advanced Scientific Research in Bengaluru\ , India. James’ work has been published in prestigious journals such as Science\, Cell\, and Nature neuroscience\, apart from other major scientif ic journals.\nSpeakers:\nAssociate Professor James P Clement Chelliah\, Ph D (Neuroscience Unit\, Jawaharlal Nehru Centre for Advanced Scientific Res earch\, Bangalore\, India) LOCATION:Sherrington Building (Sherrington Room (second floor))\, off Park s Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/84a996d7-2d8c-43c4-87a6-c842445d3838/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Small molecules that restore GABAergic function as a pote ntial therapeutics to treat Autism Spectrum Disorder - Associate Professor James P Clement Chelliah\, PhD (Neuroscience Unit\, Jawaharlal Nehru Cent re for Advanced Scientific Research\, Bangalore\, India) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:3Brain CorePlate and Accura-3D Technologies\, modern functional im aging for next-gen neuroscience - Dr Sercan Deniz (3Brain AG\, Switzerland ) DTSTART;VALUE=DATE-TIME:20220914T160000 DTEND;VALUE=DATE-TIME:20220914T170000 UID:https://talks.ox.ac.uk/talks/id/4c4a17d9-c7c3-43e4-894e-07e23cce2a3c/ DESCRIPTION:Dr Sercan Deniz will present the latest developments in high r esolution functional imaging\, with an emphasis on brain organoids\, brain slices and stem cell derived neuronal networks.\n\nMicroscopy-based high content screening approaches face many obstacles such as phototoxicity\, p hotobleaching and a low temporal resolution\, and traditional microelectro de array or patch-clamp approaches are limited by a poor spatial resolutio n.\n\n3Brain's high resolution CorePlate™ technology brings a processing core in contact with the cell network\, delivering an accurate picture of the cellular network activity\, free of speed or bandwidth constraints.\n \nAdditionally\, the latest 3D technology\, featuring thousands of penetra ting microelectrodes\, now enables the possibility of recording from insid e tissues such as brain organoids and slices.\nSpeakers:\nDr Sercan Deniz (3Brain AG\, Switzerland) LOCATION:Sherrington Building (Sherrington Room (second floor))\, off Park s Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/4c4a17d9-c7c3-43e4-894e-07e23cce2a3c/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:3Brain CorePlate and Accura-3D Technologies\, modern func tional imaging for next-gen neuroscience - Dr Sercan Deniz (3Brain AG\, Sw itzerland) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Cell-type specific responses to associative learning in the primar y motor cortex - Candice Lee (Laboratory of Simon Chen\, University of Ott awa) DTSTART;VALUE=DATE-TIME:20220916T110000 DTEND;VALUE=DATE-TIME:20220916T120000 UID:https://talks.ox.ac.uk/talks/id/3eba10bc-6233-4450-b147-ee4259c5c977/ DESCRIPTION:The primary motor cortex (M1) is known to be a critical site f or movement initiation and motor learning. Surprisingly\, it has also been shown to possess reward-related activity\, presumably to facilitate rewar d-based learning of new movements. However\, it is unclear whether and how reward-related signals are represented among different cell types in M1 d uring learning\, and which brain regions might confer this information to M1. Using in vivo two-photon calcium imaging in head-fixed mice during an associative learning task\, we found that both VIP+ and PV+ inhibitory neu rons were responsive to reward and reward-related cues. After learning\, V IP+ cells became preferentially more responsive to reward while PV+ cells became more responsive to reward-related cues. In addition\, we utilized a monosynaptic rabies tracing strategy to generate a brain-wide map of long -range input to VIP\, PV\, and SST inhibitory neurons as well as pyramidal neurons\, to identify brain regions that might confer reward-related acti vity to VIP+ cells in M1. Together\, this work uncovers neural circuits in volved in modulating M1 activity in response to reward.\nSpeakers:\nCandic e Lee (Laboratory of Simon Chen\, University of Ottawa) LOCATION:Sherrington Building (Sherrington Room (second floor))\, off Park s Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/3eba10bc-6233-4450-b147-ee4259c5c977/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Cell-type specific responses to associative learning in t he primary motor cortex - Candice Lee (Laboratory of Simon Chen\, Universi ty of Ottawa) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:High-Content Electrophysiology Platforms for Functional Characteri zation of Neurons - Dr Zhuoliang Li (MaxWell Biosystems\, Zurich\, Switzer land) DTSTART;VALUE=DATE-TIME:20220816T160000 DTEND;VALUE=DATE-TIME:20220816T170000 UID:https://talks.ox.ac.uk/talks/id/9ed530e5-340e-4d97-8bb6-0dc31574687a/ DESCRIPTION:Propagating electrical signals enable neuronal communication a nd underlie brain function. Its dysfunction\, both at a micro- and macro- scale\, plays a central role in deliberating pathologies. Therefore\, an u nrestricted access to the physiology of neurons is crucial for studying in formation processing within neuronal networks and accelerating drug develo pment for neurological disorders.\n\nHigh-density microelectrode array (HD -MEA) technology enables chronic label-free invitro extracellular recordin gs of action potentials in neurons. MaxOne (single-) and MaxTwo (multi-wel l) HD-MEA Systems (MaxWell Biosystems\, Switzerland) simultaneously captur e fast propagating action potentials across multiple neurons and enables v aluable investigation encompassing different scales\, from the network lev el\, single-cell level\, to even the sub-cellular level.\n\nEquipped with our MaxLab Live software suite\, we evaluated the neuronal activity of neu ronal cell cultures\, brain organoids\, as well as brain slices through th ree assays: (A) The ActivityScan Assay measures the overall activity and e xtract key features such as the firing rate and spike amplitude. (B) The N etwork Assay examines the synchronicity (a sign of functional connectivity ) across different neurons by investigating the network bursts. (C) Lastly \, the AxonTracking Assay automatically detects and functionally character izes axonal signals across multiple neurons.\n\nTaken together\, we showca se the capabilities of our HD-MEA platforms equipped with the MaxLab Live software suite to capture neuronal physiology across the network\, cellula r\, and sub-cellular levels for neurological disease modeling and screenin g novel therapeutic treatment strategies.\nSpeakers:\nDr Zhuoliang Li (Max Well Biosystems\, Zurich\, Switzerland) LOCATION:Sherrington Building (Florence Buchanan Lecture Theatre (second f loor))\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/9ed530e5-340e-4d97-8bb6-0dc31574687a/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:High-Content Electrophysiology Platforms for Functional C haracterization of Neurons - Dr Zhuoliang Li (MaxWell Biosystems\, Zurich\ , Switzerland) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:All-optical interrogation of the hippocampal role in episodic memo ry formation\, consolidation and retrieval - Dr Nick Robinson (University College London) DTSTART;VALUE=DATE-TIME:20220628T143000 DTEND;VALUE=DATE-TIME:20220628T153000 UID:https://talks.ox.ac.uk/talks/id/4772a334-4c4b-4e74-94fe-b3c6c8aec1ad/ DESCRIPTION:The hippocampus is crucial for spatial navigation and episodic memory formation. Hippocampal place cells exhibit spatially selective act ivity within an environment and have been proposed to form the neural basi s of a cognitive map of space that supports these mnemonic functions. Howe ver\, the direct influence of place cell activity on spatial navigation be haviour has not yet been demonstrated. Using an ‘all-optical’ combinat ion of simultaneous two-photon calcium imaging and two-photon holographica lly targeted optogenetics\, we identified and selectively activated place cells that encoded behaviourally relevant locations in a virtual reality e nvironment. Targeted stimulation of a small number of place cells was suff icient to bias the behaviour of animals during a spatial memory task\, pro viding causal evidence that hippocampal place cells actively support spati al navigation and memory. I will also describe new experiments aimed at un derstanding the fundamental encoding mechanisms that support episodic memo ry\, focussing on the role of hippocampal sequences across multiple timesc ales and behaviours. \nSpeakers:\nDr Nick Robinson (University College Lo ndon) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/4772a334-4c4b-4e74-94fe-b3c6c8aec1ad/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:All-optical interrogation of the hippocampal role in epis odic memory formation\, consolidation and retrieval - Dr Nick Robinson (Un iversity College London) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:The orexinergic signalling as a potential tool for therapeutic tar get in childhood absence epilepsy - Associate Professor Nihan Carcak Yilma z (Istanbul University Faculty of Pharmacy) DTSTART;VALUE=DATE-TIME:20220812T160000 DTEND;VALUE=DATE-TIME:20220812T170000 UID:https://talks.ox.ac.uk/talks/id/5461653c-4730-4c09-8102-23f240556ce3/ DESCRIPTION:Childhood absence epilepsy (CAE) occupies a prominent position in the genetic generalized epilepsies because CAE is a quite common\, acc ounting for 10—17% of all cases of epilepsy diagnosed in children. Orexi n\, a neuropeptide neurotransmitter that mainly regulates sleep/wake cycle \, has been shown to be involved in epilepsy. Limited data is available ab out the possible role of orexinergic system in the pathophysiology of abse nce seizures. Orexin receptors are strongly expressed in cortical neurons in the rodent brain\, and some of these neurons have extensive intracortic al and thalamic projections. Intracerebral administration of selective OX2 R agonist\, YNT-185 suppressed the cumulative duration of spontaneous abse nce seizures in genetic absence epilepsy rats (GAERS) which is the most va lidated animal model of genetic absence epilepsy. Our study revealed a sup pressive effect of OX2R agonist on absence seizures for the first time sug gesting that orexin signaling may have a modulating effect on absence seiz ures in GAERS and might be targeted by therapeutic intervention for absenc e epilepsy. The challenge is now to determine whether this effect is media ted on cortical or subcortical level. Further studies will elucidate the s tructures underlying absence seizure modulatory effect of orexin signaling . \nSpeakers:\nAssociate Professor Nihan Carcak Yilmaz (Istanbul Universit y Faculty of Pharmacy) LOCATION:Sherrington Building (Florence Buchanan Lecture Theatre (second f loor))\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/5461653c-4730-4c09-8102-23f240556ce3/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:The orexinergic signalling as a potential tool for therap eutic target in childhood absence epilepsy - Associate Professor Nihan Car cak Yilmaz (Istanbul University Faculty of Pharmacy) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Mild intrauterine hypoperfusion in rats reproduces neurodevelopmen tal disorders observed in children with fetal growth restriction - Profess or Masahiro Tsuji\, MD\, PhD (Department of Food and Nutrition\, Kyoto Wom en’s University\, Japan) DTSTART;VALUE=DATE-TIME:20220905T160000 DTEND;VALUE=DATE-TIME:20220905T170000 UID:https://talks.ox.ac.uk/talks/id/8c3f03c1-7e51-4c7a-963c-9bc0b1c0c9c5/ DESCRIPTION:Children with fetal grow restriction (FGR) and its resultant l ow birthweight (LBW) have a higher risk for developing neurodevelopmental disorders\, which include attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder. More than half of the cases of FGR are repor tedly caused by placental insufficiency\, which is a process that leads to a decrease in placental blood flow and/or transplacental transfer of oxyg en and nutrients to the fetus. Hence\, intrauterine hypoperfusion models a re probably the most important model to study the pathophysiology and cons equences of FGR-LBW. We developed a rat model of mild intrauterine hypoper fusion induced by arterial stenosis with metal microcoils wrapped around t he uterine and ovarian arteries on embryonic day 17. Most pups were born w ith significantly decreased birth weights. These LBW rat presented 1) decr eased gray and white matter areas without obvious tissue damage\, and 2) a ltered behaviors\, namely delayed newborn reflexes\, hyperactivity\, and l ack of sociability. We have been investigating the pathophysiology of the FGR-LBW rats and found that they exhibit\, for instance\, 1) mild inflamma tion in placenta\, 2) diminished post-active depression\, and 3) altered l evels and distributions of metabolites in the brain. This model mimics the clinical signs and symptoms of children with neurodevelopmental disorders born FGR-LBW and could be a useful model to study the mechanisms of FGR-L BW harmful effects and to develop therapeutic interventions for the disord ers.\nSpeakers:\nProfessor Masahiro Tsuji\, MD\, PhD (Department of Food a nd Nutrition\, Kyoto Women’s University\, Japan) LOCATION:Sherrington Building (Blakemore Lecture Theatre)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/8c3f03c1-7e51-4c7a-963c-9bc0b1c0c9c5/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Mild intrauterine hypoperfusion in rats reproduces neurod evelopmental disorders observed in children with fetal growth restriction - Professor Masahiro Tsuji\, MD\, PhD (Department of Food and Nutrition\, Kyoto Women’s University\, Japan) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Gene-environment interactions modulating brain function within and between generations - Professor Anthony J. Hannan (Florey Institute of Ne uroscience and Mental Health\, University of Melbourne) DTSTART;VALUE=DATE-TIME:20220615T160000 DTEND;VALUE=DATE-TIME:20220615T170000 UID:https://talks.ox.ac.uk/talks/id/055675ae-785b-428b-8bec-b0d0c7b3b410/ DESCRIPTION:Each of us can trace our origins from conception\, with the in formation in our genomes and epigenomes guiding development\, and environm ental factors modulating this trajectory over time. We have been intereste d in how genes and environment combine to sculpt brain development and fun ction\, in health and disease. We have examined the role of various molecu lar and cellular mediators\, and environmental modulators\, as they influe nce healthy cognitive and affective function on the one hand\, and cogniti ve and affective disorders on the other.\n\nHuntington’s disease (HD) is one of over 50 tandem-repeat disorders and involves neurodegeneration lea ding to psychiatric\, cognitive and motor symptoms. In a preclinical model of HD\, expressing the tandem-repeat mutation\, we have demonstrated that environmental enrichment (enhanced cognitive stimulation and physical act ivity) can delay onset of endophenotypes modelling depression\, dementia a nd movement disorders. These findings have been extended to include stress and exercise interventions\, and environmental manipulations in models of other neurological and psychiatric disorders\, including autism\, schizop hrenia\, depression and anxiety disorders. Our molecular and cellular inve stigations have revealed key pathways implicated in the therapeutic impact s of environmental stimuli and identified novel therapeutic targets. We ha ve also discovered altered brain-body interactions\, including the first e vidence of gut dysbiosis (dysregulated microbiota) in HD\, and a preclinic al model of schizophrenia. Ongoing studies are exploring the gut microbiom e as a therapeutic target and the possibility that specific environmental factors may modulate brain function via microbiota-gut-brain interactions. These approaches to gene-environment interactions may facilitate the deve lopment of enviromimetics (including exercise mimetics as a subclass) for a variety of brain disorders known to be modulated by environmental stimul i.\n\nIn a parallel program of research\, we have been exploring epigeneti c inheritance via the paternal lineage. We have discovered the transgenera tional effects of various paternal environmental exposures. Our findings r eveal significant experience-dependent effects on cognitive and affective function of offspring via epigenetic inheritance. We are investigating the impacts of specific environmental and pharmacological factors\, including exercise and stress-hormone elevation\, and the relevance of these discov eries in mice to human transgenerational epigenetics and associated ‘epi genopathy’. Our ongoing studies are exploring mechanisms whereby experie nce can modify germ cells and associated sperm epigenetics\, and how these epigenetic modifications (of mice and men) may modulate offspring phenoty pes and their potential susceptibility to various brain disorders.\nSpeake rs:\nProfessor Anthony J. Hannan (Florey Institute of Neuroscience and Men tal Health\, University of Melbourne) LOCATION:Sherrington Building (Blakemore Lecture Theatre)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/055675ae-785b-428b-8bec-b0d0c7b3b410/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Gene-environment interactions modulating brain function w ithin and between generations - Professor Anthony J. Hannan (Florey Instit ute of Neuroscience and Mental Health\, University of Melbourne) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Photobiomodulation for neurodegenerative disease: a journey from b ench to clinic - Professor John Mitrofanis (Université Grenoble Alpes Sai nt Martin d'Hères\, France\, and University College London\, UK) DTSTART;VALUE=DATE-TIME:20220318T110000Z DTEND;VALUE=DATE-TIME:20220318T120000Z UID:https://talks.ox.ac.uk/talks/id/d175cac5-d9db-4f93-95c2-92b71f41d7b1/ DESCRIPTION:This seminar takes you on a journey\, tracing the history of a somewhat serendipitous finding in the laboratory\, to the translation of this finding to the clinic and its use on patients. The journey starts wit h a discussion over a cup of coffee between two old friends. They devised an experiment using a photobiomodulation device\, one that delivered red t o near-infrared light\, on a few spare parkinsonian mice left over from ot her experiments. The thinking was that because photobiomodulation stimulat es mitochondrial function\, it may improve the mitochondrial dysfunction a nd protect neurones against the parkinsonian insult. After a week or so\, it turned out that these photobiomodulation-treated mice had more survivin g neurones than those that were not treated\; in addition\, they were foun d to have improved locomotor behaviour. This led to explorations in non-hu man primates\, the gold-standard of all animal models of the disease. Here \, in this species\, the same beneficial outcomes were found\, namely\, le ss pathology and improved clinical signs. These experimental findings led to clinical interest and\, as it stand now\, clinical trials are underway testing the efficacy of several photobiomoduation approaches in Parkinson' s disease patients. There are also encouraging\, early indications that ph otobiomodulation is effective in Alzheimer's disease\, with both neuroprot ective and positive cognitive behavioural outcomes being evident in mouse models of the disease. We are in the process of starting a new series of s tudies that test the efficacy of photobiomodulation in Alzheimer's disease further\, in both animal models and in patients.\nSpeakers:\nProfessor Jo hn Mitrofanis (Université Grenoble Alpes Saint Martin d'Hères\, France\, and University College London\, UK) LOCATION:Sherrington Building (Florence Buchanan Lecture Theatre (second f loor))\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/d175cac5-d9db-4f93-95c2-92b71f41d7b1/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Photobiomodulation for neurodegenerative disease: a journ ey from bench to clinic - Professor John Mitrofanis (Université Grenoble Alpes Saint Martin d'Hères\, France\, and University College London\, UK) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Body Brain Behavior - The Need For Conversations - Professor Zolta n Molnar (DPAG\, University of Oxford)\, Tamas Horvath\, DVM\, PhD (Yale S chool of Medicine)\, Joy Hirsch\, PhD (Yale School of Medicine) DTSTART;VALUE=DATE-TIME:20220407T160000 DTEND;VALUE=DATE-TIME:20220407T170000 UID:https://talks.ox.ac.uk/talks/id/3c757a23-fe87-4b67-bc5b-0c8f60d6d1cc/ DESCRIPTION:"Body\, Brain\, Behavior: Three Views and a Conversation" desc ribes brain research on the frontiers\, with a particular emphasis on the relationship between the brain and its development and evolution\, periphe ral organs\, and other brains in communication. The book expands current v iews of neuroscience by illustrating the integration of these disciplines. By using a novel method of conversations between 3 scientists of differen t disciplines\, cellular\, endocrine\, developmental\, and social processe s are seamlessly woven into topics that relate to contemporary living in h ealth and disease. This book is a critical read for anyone who wants to be come familiar with the inner workings of the nervous system and its intima te connections to the universe of contemporary life issues. This pioneerin g book does the following:\n\n- Introduces the reader to basic principles of brain research and integrative physiology.\n\n- Dissects the dispute be tween Cajal and Golgi regarding the state-of-the art in the neurosciences and immunobiology.\n\n- Provides a short history of brain research and met abolism.\n\n- Discusses contemporary approaches in the neurosciences\, alo ng with the importance of technological versus conceptual advances.\n\n- E xamines the dynamics of social connections between two brains\, integratin g mechanisms of Body/Brain/Behavior-to-Body/Brain/Behavior between subject s.\n\nTo launch the book in Oxford\, talks will be given by each of the th ree authors to outline their perspectives:\n\nTamás Horváth: "The hunger view on body\, brain and behavior"\n\nJoy Hirsch: "Brain-to-Brain"\n\nZol tán Molnár: "The developing brain"\n\nThe lectures will be followed by r eception in the Sherrington reception foyer 5-6pm\n\n"This book illustrate s how natural dialogue between scientists from diverse areas of interest a nd scholarship related to body\, brain\, and behavior serves as a web to c onnect elemental topics into a global Neuroscience of Life" - Joy Hirsch\, PHD\n\nRead more about the book on the DPAG website: https://www.dpag.ox. ac.uk/news/new-book-expands-the-horizons-of-brain-research\n\nThe book is available to purchase on the Elsevier website: https://www.elsevier.com/bo oks/body-brain-behavior/horvath/978-0-12-818093-8\nSpeakers:\nProfessor Zo ltan Molnar (DPAG\, University of Oxford)\, Tamas Horvath\, DVM\, PhD (Yal e School of Medicine)\, Joy Hirsch\, PhD (Yale School of Medicine) LOCATION:Sherrington Building (Blakemore Lecture Theatre)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/3c757a23-fe87-4b67-bc5b-0c8f60d6d1cc/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Body Brain Behavior - The Need For Conversations - Profes sor Zoltan Molnar (DPAG\, University of Oxford)\, Tamas Horvath\, DVM\, Ph D (Yale School of Medicine)\, Joy Hirsch\, PhD (Yale School of Medicine) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:5-HT in the medial septum regulates social memory - Dr Xiaoting Wu \, Ph.D. (Stanford University) DTSTART;VALUE=DATE-TIME:20220118T160000Z DTEND;VALUE=DATE-TIME:20220118T170000Z UID:https://talks.ox.ac.uk/talks/id/507667bf-1e01-4bc4-b633-413a957324ef/ DESCRIPTION:The ability to remember familiar conspecifics\, termed social memory\, is critical for an animal’s behaviour in its social environment . In recent years\, extensive evidence supports the importance of distinct hippocampal subregions\, dorsal CA2 (dCA2) and ventral CA1 (vCA1) in the regulation of social memory. However\, little is known about the relevant input regions. Here\, we present evidence that the medial septum (MS)\, se nds inputs to the hippocampus that are required for social memory. Further more\, we find that 5-HT modulation of the MS bi-directionally influences social memory formation. \n\nUsing TRAP2\;Ai14 mice as an unbiased approac h for identifying dCA2 and vCA1 input regions that are activated during so cial encounters\, we identified elevated activity in the MS. Inhibition of the MS→dCA2 projection\, but not the MS→vCA1 projection impaired soci al memory. Strikingly\, excitation of the MS can prolong social memory. Mo reover\, we show elevated MS cell activity during social interactions\, wh ich is modulated by 5-HT1b receptors (R) and 5-HT release from the median raphe. This elevated activity in turn plays a role in establishing plastic ity in the downstream dCA2 pyramidal neurons\, a process crucial for socia l memory formation. Surprisingly\, a 5-HT1bR agonist infused into the MS c an prolong social memory in wild-type mice and rescue social memory defici ts in an autism-associated mouse model with social memory deficits. This f inding may prove therapeutically beneficial since social memory is commonl y impaired in autism. Together these findings reveal a 5-HT modulated MS →dCA2 circuit that is required for the regulation of social memory.\nSpe akers:\nDr Xiaoting Wu\, Ph.D. (Stanford University) LOCATION:This seminar will be held on Microsoft Teams. Please email hod-pa @dpag.ox.ac.uk for more details and the link to join. TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/507667bf-1e01-4bc4-b633-413a957324ef/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:5-HT in the medial septum regulates social memory - Dr Xi aoting Wu\, Ph.D. (Stanford University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:"Popsee" unveiling by Patrick Hughes in honour of Sir Colin Blakem ore - Patrick Hughes (Artist) DTSTART;VALUE=DATE-TIME:20211102T163000Z DTEND;VALUE=DATE-TIME:20211102T173000Z UID:https://talks.ox.ac.uk/talks/id/445919c0-0078-44e6-8f9e-803e6897c0af/ DESCRIPTION:An artwork entitled "Popsee" has been donated to the Departmen t of Physiology\, Anatomy and Genetics (DPAG) by British artist Patrick Hu ghes in honour of Emeritus Professor of Physiology Sir Colin Blakemore FR S and their shared interest in visual perception. \n\nPatrick Hughes was b orn in Birmingham\, England in October 1939. His first exhibition was in 1 961 and his first reverspective\, Sticking-out Room\, was made in 1964. Hu ghes' original painted reliefs are concerned with optical and visual illus ions\, the science of perception and the nature of artistic representation . He invented an optical illusion called “reverspective\,” a neologism for reverse perspective. Hughes begins by constructing pyramid- or wedge- shaped blocks out of wood\, which he combines into ridged panoramas. He th en paints scenes into the blocks\, depicting interior spaces—including m useum galleries hung with iconic artworks—as well as landscapes and city views. The protruding parts of the works appear to recede\, and the reced ing parts appear to protrude. As viewers walk by the pieces\, the composit ions seem to move.\n\nHughes' "Popsee" is an awe inspiring 3D Multiple\, h and painted\, pop culture inspired\, three dimensional piece. It incorpora tes work by Warhol\, Vasarely\, Thiebaud\, Hughes\, Lichtenstein\, Koons\, Banksy\, Haring\, and finally Signac’s iconic painting of Félix Féné on\, the art dealer\, anarchist activist and critic who coined the term Ne o-Impressionism to describe the works of Signac and Seurat in the late 189 0s. Of particular note to the neuroscience community is a book within the picture featuring Professor Blakemore's name.\n\nSir Colin Blakemore is a world-renowned neuroscientist who has significantly contributed to our und erstanding of vision\, and how the brain develops and adapts. He has been influential in demonstrating ‘neural plasticity’ — how brain cells r eorganise themselves in response to the environment after birth and even i n adulthood. Professor Blakemore joined the Department in October 1979 at the age of 35 years as the youngest Waynflete Chair of Physiology and a Pr ofessorial Fellowship at Magdalen College\, positions he held until July 2 007. During this time\, he directed the McDonnell-Pew Centre for Cognitive Neuroscience and the Oxford Centre for Cognitive Neuroscience. From 2007- 12\, he was Professor of Neuroscience at the University of Oxford and Supe rnumerary Fellow at Magdalen. Professor Blakemore\, who remains Emeritus P rofessor at DPAG\, is also very well known for his passionate belief in th e importance of public engagement with research. He has held several influ ential positions\, including serving as Chief Executive of the Medical Res earch Council from 2003-07\, and received a knighthood in 2014 for service s to scientific research\, policy and outreach.\n\nOn Tuesday 2 November 2 021\, an unveiling ceremony presented by the artist will take place\, foll owed by a drinks reception\, in the Sherrington Building Foyer.\nSpeakers: \nPatrick Hughes (Artist) LOCATION:Sherrington Building (Sherrington Foyer)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/445919c0-0078-44e6-8f9e-803e6897c0af/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:"Popsee" unveiling by Patrick Hughes in honour of Sir Col in Blakemore - Patrick Hughes (Artist) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Engineered gene delivery vectors and microbial opsins for precise and minimally-invasive study and repair of nervous systems - Viviana Gradi naru (California Institute of Technology) DTSTART;VALUE=DATE-TIME:20210628T130000 DTEND;VALUE=DATE-TIME:20210628T140000 UID:https://talks.ox.ac.uk/talks/id/6fffbeb2-e839-474d-b1c9-d217a2f13109/ DESCRIPTION:To access the lecture online via Teams: https://tinyurl.com/58 bus8p9 \n\nSPEAKER BIOGRAPHY\n\nDr Viviana Gradinaru completed her B.S. at Caltech and her Ph.D. research at Stanford University and is now a Profes sor of Neuroscience and Biological Engineering at Caltech. Prof Gradinaru has more than 70 publications in top peer-reviewed journals and more than 10 granted patents\, additional pending\, in areas of optogenetics\, viral vectors\, and tissue clearing and imaging. Prof Gradinaru has received th e NIH Director’s New Innovator and Pioneer Awards and a Presidential Ear ly Career Award for Scientists and Engineers\, and has been honored as a W orld Economic Forum Young Scientist. Gradinaru is also a Sloan Fellow\, Pe w Scholar\, Moore Inventor\, Vallee Scholar\, and Allen Brain Institute Co uncil Member\, and received the inaugural Peter Gruss Young Investigator A ward by the Max Planck Florida Institute for Neuroscience. In 2017 she was the Early-Career Scientist Winner in the Innovators in Science Award in N euroscience (Takeda and the New York Academy of Sciences)\; in 2018 she re ceived a Gill Transformative award\; in 2019 Gradinaru was a Life Sciences Finalist for the Blavatnik National Awards for Young Scientists\; and in 2020 she was the winner of Science Magazine & PINS Prize for Neuromodulati on and awarded: the Vilcek Prize for Creative Promise in Biomedical Scienc e\; the Outstanding New Investigator Award by the American Society of Gene and Cell Therapy\; and the Society for Neuroscience Young Investigator Aw ard.\n\nProfessor Gradinaru teaches undergraduate and graduate level class es on viral biology and optogenetics techniques in neuroscience. Viviana G radinaru has also been very active in technology dissemination\, participa ting with lab members in regular technology training workshops at Caltech and for summer courses at Cold Spring Harbor Laboratory as well as foundin g and now advising the CLOVER Center (Beckman Institute for CLARITY\, Opto genetics and Vector Engineering)\, which provides training and access to t he group's reagents and methods for the broader research community (awarde d Addgene Blue Flame for reagent dissemination). Gradinaru is also a cofou nder and board member of Capsida Biotherapeutics\, a fully integrated AAV engineering and gene therapy company.\n\nRESEARCH SUMMARY\n\nDr Gradinaru ’s research group at Caltech specializes in developing neuroscience tool s and methods\, including engineering of new viral vectors with optimized brain tropism after systemic delivery. In addition to developing technolog ies for neuroscience\, Dr Gradinaru has also been using such tools and met hods to dissect circuitry underlying movement\, mood\, and sleep disorders (Gradinaru et al.\, Science\, 2009\; Xiao et al\, Neuron\, 2016\; Cho et al\, Neuron\, 2017\; Oikonomou et al\, Neuron\, 2019). The Gradinaru group at Caltech has recently developed and disseminated various new tools for less invasive gene delivery and optogenetics to the brain (Deverman et al Nature Biotechnology 2016\; Chan et al Nature Neuroscience 2017\; Challis and Kumar et al Nature Protocols 2019\; Bedbrook et al Nature Methods 2020 \; Kumar et al Nature Methods 2020). With collaborators and her own Caltec h group\, Dr Gradinaru is now applying these gene delivery tools to neurod evelopmental and neurodegenerative disorders (Challis et al Nature Neurosc ience 2019\; Rauch et al Nature 2020).\nSpeakers:\nViviana Gradinaru (Cali fornia Institute of Technology) LOCATION:Sherrington Building (Viewing is online via Microsoft Teams)\, of f Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/6fffbeb2-e839-474d-b1c9-d217a2f13109/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Engineered gene delivery vectors and microbial opsins for precise and minimally-invasive study and repair of nervous systems - Vivi ana Gradinaru (California Institute of Technology) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Developing approaches to explore proteome complexity in the human brain - Dr Becky Carlyle (Massachusetts General Hospital\, Harvard Univers ity) DTSTART;VALUE=DATE-TIME:20210511T150000 DTEND;VALUE=DATE-TIME:20210511T160000 UID:https://talks.ox.ac.uk/talks/id/7f84ae4f-8e45-4b68-9720-76c626f00951/ DESCRIPTION:The explosion of new functional genomic technologies has revol utionised our approach to systems biology and highlighted a number of nove l targets in neurodegenerative and\, to a lesser extent\, psychiatric dise ases. However\, the exact structure of a protein\, its sub-cellular locat ion\, and post-translation modifications are critical to defining its func tion. Traditionally these properties have been defined through focused ch aracterization of a single protein or protein complex. Mass-spectrometry p roteomics enables high-throughput profiling of the larger proteome\, but i s often applied to bulk tissue\, with quantification summarised to the lev el of protein groups. Here I will argue that this level of analysis inade quately captures the complexity of protein abundance in the human brain\, and will talk about my experience developing methods to improve the resolu tion of proteomic techniques. I will describe analytical approaches to qu antification of protein isoforms via the integration of high-throughput tr anscriptomics and proteomics\, and the use of biochemical methods for the sub-cellular localisation of proteins in post-mortem human tissue. \nSpeak ers:\nDr Becky Carlyle (Massachusetts General Hospital\, Harvard Universit y) LOCATION:This seminar will be held on Microsoft Teams. Please email hod-pa @dpag.ox.ac.uk for more details and the link to join. TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/7f84ae4f-8e45-4b68-9720-76c626f00951/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Developing approaches to explore proteome complexity in t he human brain - Dr Becky Carlyle (Massachusetts General Hospital\, Harvar d University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:The Many Layers of Tactile Sensation - Randy M. Bruno\, Ph.D. (Dep t. of Neuroscience\, Zuckerman Mind Brain Behavior Institute\, Columbia Un iversity) DTSTART;VALUE=DATE-TIME:20210408T143000 DTEND;VALUE=DATE-TIME:20210408T153000 UID:https://talks.ox.ac.uk/talks/id/5a1f4f9b-a9ff-4daa-8601-3a24c4d340ef/ DESCRIPTION:The neocortex is critical to human and animal cognition—brea thtakingly encompassing sensation\, perception\, decision making\, and mov ement. These diverse functions are achieved by highly stereotyped circuitr y that nature appears to have iterated across the entire surface of the br ain. Dysfunction of cortical circuits contributes to numerous neurological and psychiatric disorders. We previously showed that ascending signals fr om thalamus are copied separately to the superficial and deep layers of se nsory cortex. These two halves of neocortex appear able to function indepe ndently despite their dense interconnections. We are presently investigati ng the necessity of the primary somatosensory cortex and its constituent l ayers and cell types in various tactile object recognition behaviors\, bot h published and unpublished. I will show how modern optogenetic and older lesion approaches can lead to radically different conclusions about necess ity of a brain structure or cell type to a behavior. We have found that se nsory cortex is dispensable for learning and performing some of the field ’s most widely used behavioral paradigms. This underscores the competenc y of subcortical systems at basic behavioral tasks and suggests alternativ e scenarios by which cortex and its layers contribute to complex behavior. I will also show how learning alters apical dendrites in cortical layer 1 as new behaviors are acquired.\nSpeakers:\nRandy M. Bruno\, Ph.D. (Dept. of Neuroscience\, Zuckerman Mind Brain Behavior Institute\, Columbia Unive rsity) LOCATION:This seminar will be held on Microsoft Teams. Please email hod-pa @dpag.ox.ac.uk for more details and the link to join. TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/5a1f4f9b-a9ff-4daa-8601-3a24c4d340ef/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:The Many Layers of Tactile Sensation - Randy M. Bruno\, P h.D. (Dept. of Neuroscience\, Zuckerman Mind Brain Behavior Institute\, Co lumbia University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Epigenetic and transcriptional regulation of neuronal circuit deve lopment and maturation - Taro Kitazawa\, Ph.D. (Friedrich Miescher Institu te for Biomedical Research) DTSTART;VALUE=DATE-TIME:20210304T143000Z DTEND;VALUE=DATE-TIME:20210304T153000Z UID:https://talks.ox.ac.uk/talks/id/3eb5014f-73f3-40a7-b052-747c27b6b053/ DESCRIPTION:Appropriate transcriptional responses to environmental stimuli are fundamental for cellular development and maturation. In developing se nsory neurons\, neuronal activity-response genes are induced at birth by s ensory experience\, which drives neuronal maturation. In this seminar\, fi rstly I will talk about how chromatin states regulate this transcriptional program during development. To address this issue\, we isolated barrelett e neurons (whisker-associated sensory neurons) from developing mouse hindb rains in wild-type and activity-deprived conditions using ad hoc genetic t ools\, and carried out chromatin and transcriptional profiling. We found t hat prior to perinatal induction immediate early genes (IEGs) are embedded into a unique ‘bipartite’ Polycomb chromatin signature. Namely\, they carry active H3K27ac on promoters and enhancers\, but repressive Ezh2-dep endent H3K27me3 on gene bodies. This bipartite chromatin signature is not only found in neurons but it is widely present in developing cell types\, including embryonic stem cells\, and originates from bivalent chromatin. P olycomb marking of gene bodies inhibits productive mRNA elongation resulti ng in immature transcripts of bipartite genes\, despite active promoters a nd enhancers\, dampening basal productive transcription while maintaining their potential for fast induction. We revealed an epigenetic mechanism re gulating the rapidity and amplitude of the transcriptional response to rel evant stimuli\, while preventing inappropriate activation of stimulus resp onse genes and downstream cellular maturation programs.\n\nLastly\, I will also briefly introduce about my future research project\, in which I aim to decipher the developmental and molecular basis how a spatially intermin gled and homogeneous neuronal population generates heterogeneous identitie s regarding circuit wring. To achieve this research goal\, I will develop a novel retrospective genomics approach to overcome a critical bottleneck of the current snapshot-type of sequencing technologies.\nSpeakers:\nTaro Kitazawa\, Ph.D. (Friedrich Miescher Institute for Biomedical Research) LOCATION:This seminar will be held on Microsoft Teams. Please email hod-pa @dpag.ox.ac.uk for more details and the link to join. TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/3eb5014f-73f3-40a7-b052-747c27b6b053/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Epigenetic and transcriptional regulation of neuronal cir cuit development and maturation - Taro Kitazawa\, Ph.D. (Friedrich Miesche r Institute for Biomedical Research) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Striatal activity topographically reflects cortical activity - Dr Andrew Peters (UCL) DTSTART;VALUE=DATE-TIME:20210119T150000Z DTEND;VALUE=DATE-TIME:20210119T160000Z UID:https://talks.ox.ac.uk/talks/id/e9df1b71-7268-455b-be40-2050fa393d89/ DESCRIPTION:The dorsal striatum receives a major and topographic input fro m the cortex\, and the cortex and striatum are thought to work together to carry out a diverse set of functions. It is unclear how the cortex and st riatum influence each other however\, and it has been suggested that each carries distinct sensorimotor correlates to serve complementary roles. We sought to record from connected regions of the cortex and striatum in mice during sensory guided behavior to determine the relationship of activity across structures. We found precise spatial correlations in activity follo wing anatomical projections from the cortex to the striatum\, and activity in the striatum reflected that in associated cortical regions consistentl y across behavioral contexts. This match in activity was scaled by learnin g\, as untrained mice exhibited smaller sensory responses selectively in t he striatum. These results suggest a simple and scalable mapping of activi ty between the cortex and striatum.\nSpeakers:\nDr Andrew Peters (UCL) LOCATION:This seminar will be held on Microsoft Teams. Please email hod-pa @dpag.ox.ac.uk for more details and the link to join. TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/e9df1b71-7268-455b-be40-2050fa393d89/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Striatal activity topographically reflects cortical activ ity - Dr Andrew Peters (UCL) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Biologist\, Know Thy Cells - A Colorful Barcoding Method to ID Cel l Types\, their Fate\, and Decode Brainwide Communication - Dr Eviatar Yem ini (Columbia University) DTSTART;VALUE=DATE-TIME:20201125T150000Z DTEND;VALUE=DATE-TIME:20201125T160000Z UID:https://talks.ox.ac.uk/talks/id/519cbb46-f2c8-4d1f-9bf1-95c762c74b53/ DESCRIPTION:A major challenge in biological imaging is resolving cell iden tities. These are necessary for determining cell-specific protein expressi on and function\, the effect of transcription factors on cell fate\, and t he contribution of individual neurons to brainwide activity and behavior. Present methods are limited to a piecemeal approach\, using multiple strai ns to identify a few cell types at a time. I introduce a new method and so ftware that can identify many cell types\, and in some cases all neurons\, in vivo using a single strain. My method combines cell reporters with fiv e distinguishable fluorescent proteins to create unique\, stereotyped colo r codes that identify cell types. I illustrate this in C. elegans\, engine ering a multicolor transgene called NeuroPAL (a Neuronal Polychromatic Atl as of Landmarks)\, to create an identical colormap in all worms that uniqu ely identifies every neuron\, showcasing three applications. First\, I ide ntify the neuronal expression patterns of all metabotropic receptors for a cetylcholine\, GABA\, and glutamate\, thus completing a map of this commun ication network. My findings indicate that second-messenger systems are th e primary means of GABA communication in worm\, and further suggest widesp read extrasynaptic GABA signaling. Second\, I analyze the conserved transc ription factor EOR-1/PLZF and\, despite its ubiquitous expression\, uncove r a precise role in neuronal fate. Third\, I identify brainwide codes for gustatory and olfactory stimuli. My findings show a complex code that chal lenges the present view that global neuronal activity is simply low dimens ional. To facilitate the workflow\, I present semi-automated cell identifi cation software and optimal-coloring software to apply the same method in other tissues and organisms. Lastly\, I discuss future applications: inves tigating how whole-nervous-system activity is remodeled to change behavior during early development\, sexual maturation\, in response to environment al stress\, and even across 15+ million years of evolutionary divergence.\ nSpeakers:\nDr Eviatar Yemini (Columbia University) LOCATION:This seminar will be held on Microsoft Teams. Please email hod-pa @dpag.ox.ac.uk for more details and the link to join. TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/519cbb46-f2c8-4d1f-9bf1-95c762c74b53/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Biologist\, Know Thy Cells - A Colorful Barcoding Method to ID Cell Types\, their Fate\, and Decode Brainwide Communication - Dr Ev iatar Yemini (Columbia University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Mechanisms of plasticity in visual circuits - Prof Leon Lagnado FM edSci (School of Life Sciences\, University of Sussex) DTSTART;VALUE=DATE-TIME:20200302T120000Z DTEND;VALUE=DATE-TIME:20200302T130000Z UID:https://talks.ox.ac.uk/talks/id/87a7fc6b-a5d0-41b8-b28a-f96d00b5819e/ DESCRIPTION:The sensory world is constantly changing and neural circuits m ust adapt to these changes if information is to be extracted efficiently. But the processing of external stimuli is also modulated by changes in th e internal state of the animal\, reflected in the sleep-wake cycle\, motor activity and arousal. In this presentation I will describe how we have u sed in vivo imaging to investigate the mechanisms by which these external and internal factors adjust visual processing in the retina and cortex. O ne focus will be the varied roles of inhibitory interneurons and a second will be the actions of the neuromodulator dopamine on the synaptic machine ry that transmits the visual signal. \nSpeakers:\nProf Leon Lagnado FMedS ci (School of Life Sciences\, University of Sussex) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/87a7fc6b-a5d0-41b8-b28a-f96d00b5819e/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Mechanisms of plasticity in visual circuits - Prof Leon L agnado FMedSci (School of Life Sciences\, University of Sussex) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Human adult hippocampal neurogenesis during physiological and path ological aging - Professor Maria Llorens-Martín (Department of Molecular Neuropathology\, Centro de Biología Molecular “Severo Ochoa” Madrid) DTSTART;VALUE=DATE-TIME:20191211T120000Z DTEND;VALUE=DATE-TIME:20191211T130000Z UID:https://talks.ox.ac.uk/talks/id/cd10688e-bdb8-4a86-a0b6-ebd516006d67/ DESCRIPTION:The hippocampus\, a brain region crucial for learning and memo ry hosts one of the most unique phenomena of the adult mammalian brain\, n amely the addition of new neurons throughout lifetime. Memory impairment i n Alzheimer’s Disease (AD) can be attributed to a significant decline in the functioning of the hippocampal formation. Studies in mice suggest tha t the disease could also target the generation of new neurons – or adult hippocampal neurogenesis (AHN). In this talk\, I will revisit the occurre nce of continued neurogenesis in the human hippocampus of aged healthy sub jects and patients with neurodegenerative diseases\, using brain material obtained under tightly controlled conditions and applying state-of-the-art tissue processing methods. Our data evidence that AHN is a robust phenome non in the human brain\, and points to impaired neurogenesis as a potentia lly relevant mechanism underlying AD that may be amenable to novel therape utic strategies. \nSpeakers:\nProfessor Maria Llorens-Martín (Department of Molecular Neuropathology\, Centro de Biología Molecular “Severo Ocho a” Madrid) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/cd10688e-bdb8-4a86-a0b6-ebd516006d67/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Human adult hippocampal neurogenesis during physiological and pathological aging - Professor Maria Llorens-Martín (Department of M olecular Neuropathology\, Centro de Biología Molecular “Severo Ochoa” Madrid) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:A normative perspective on the diversity of dopamine neurons - Pro fessor Naoshige Uchida (Harvard University) DTSTART;VALUE=DATE-TIME:20191204T160000Z DTEND;VALUE=DATE-TIME:20191204T170000Z UID:https://talks.ox.ac.uk/talks/id/516931fa-9410-441d-b33b-e9d5479e6ab4/ DESCRIPTION:Midbrain dopamine neurons play important roles in learning\, m otivation and movements. It has long been thought that dopamine neurons br oadcast a reward prediction error signal to drive learning to predict futu re outcomes. Recent studies have shown\, however\, that the signals sent b y dopamine neurons are more diverse than previously thought. For instance\ , some dopamine neurons are activated by threatening stimuli but not by re ward. It has been postulated that the activity of some dopamine neurons ma y be correlated with movement kinematics (e.g. speed) or the distance to a reward location (or motivational value) but not with reward prediction er rors. These results have been taken as evidence that challenges the canoni cal view of dopamine signals based on reward prediction errors. In this ta lk\, I will try to present a normative perspective on these diverse dopami ne signals under the framework of the reinforcement learning theory.\nSpea kers:\nProfessor Naoshige Uchida (Harvard University) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/516931fa-9410-441d-b33b-e9d5479e6ab4/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:A normative perspective on the diversity of dopamine neur ons - Professor Naoshige Uchida (Harvard University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Joint Meeting of Oxford Neuroscience & Neurocure Cluster of Excell ence\, Charité Universitätsmedizin\, Berlin DTSTART;VALUE=DATE-TIME:20191122T090000Z DTEND;VALUE=DATE-TIME:20191122T190000Z UID:https://talks.ox.ac.uk/talks/id/fe66c928-abdf-4024-9791-87eea2c1dd28/ DESCRIPTION:MECHANISMS OF SYNAPTIC RELEASE AND SECRETION \n\n9:00 – 9:05 Zoltán Molnár and Alastair M. Buchan\, Department of Physiology\, Anato my and Genetics\, University of Oxford and Radcliffe Department of Medicin e\, University of Oxford. Introduction\n\n9:05 – 9:30 Maike Glitsch\, De partment of Physiology\, Anatomy and Genetics\, University of Oxford. “I mpact of sex and cell shape on intracellular Ca2+ signals in brain cells ” \n\n9:30 – 9:55 Gregor Sachse\, (Fran Aschcroft Group) Department of Physiology\, Anatomy and Genetics\, University of Oxford. “Look\, don' t touch - microcompartment \nelectrophysiology studied with optogenetic to ols” \n\n9:55 – 10:20 Alex Jeans\, Department of Pharmacology\, Unive rsity of Oxford. “Synaptic release in disease”\n\n10:20 – 10:45 Coff ee\n\n10:45 – 11:10 Clive Wilson\, Department of Physiology\, Anatomy an d Genetics\, University of Oxford. “Fundamental mechanisms of regulated secretion and exosome release”\n\n11:10 – 11:35 Ed Mann\, Department o f Physiology\, Anatomy and Genetics\, University of Oxford. “Over-expres sion of GluA2 in hippocampal parvalbumin-expressing interneurons leads to memory interference”\n\n11:35 – 12:30 ROUNDTABLE DISCUSSION - interact ions between Oxford Neuroscience & Neurocure Cluster of Excellence\, Chari té Universitätsmedizin\, Berlin: “Introductions to Neuroscience at Ber lin and Oxford” \nChristian Rosenmund\, Charité - Universitätsmedizin Berlin\, CC02 für Grundlagenmedizin Neurowiss. für zelluläre molek. Neu robiologie -AG Rosenmund-\nCharitéplatz 1\, 10117 Berlin\, Germany. \nMat thew Larkum\, Humboldt University\, Berlin\, Neurocure Cluster of Excellen ce\, Neuroscience Research Center – Campus Mitte\; Charité Universität smedizin Berlin\nAndrew King\, Department of Physiology\, Anatomy and Gene tics\, University of Oxford\n\nDPAG HoD SEMINAR Large Lecture Theatre\, Sh errington Building\, DPAG:\n1:00 – 2:00 Christian Rosenmund\, Charité - Universitätsmedizin Berlin\, CC02 für Grundlagenmedizin Neurowiss. für zelluläre molek. Neurobiologie -AG Rosenmund-\nCharitéplatz 1\, 10117 B erlin\, Germany. “Architectural principles in central mammalian synapses "\n\n2:00 – 3:00 LUNCH (Sherrington Library) Sponsored by DPAG Neuroscie nce\n\nMECHANISMS OF BRAIN STATE CONTROL \n\n3:00 – 3:30 Timothy Zolnik (Larkum Laboaratory) Humboldt University\, Berlin\, Neurocure Cluster of E xcellence\, Neuroscience Research Center – Campus Mitte\; Charité Unive rsitätsmedizin Berlin “Integration and non-linear signalling among comp lex dendrites of cortical neurons\, and synaptic interactions in cortical networks with special attention to layer 6b neurons”\n \n3:30 – 3:50 A nna Hoerder-Suabedissen (Molnár & Szele Laboratories) Department of Physi ology\, Anatomy and Genetics\, University of Oxford. “Layer 6b\, a corti cal layer with no known function” \n\n3:50 – 4:10 Tea\n\n4:10 – 4:30 Filippo Ghezzi (Butt & Packer Laboratories) Department of Physiology\, An atomy and Genetics\, University of Oxford. “Lpar1-EGFP subplate neurons represent two distinct subtypes with contrasting roles in early postnatal somatosensory cortex”\n\n4:30 – 4:50 Lukas B. Krone (Vyazovskiy & Moln ár Laboratories) Department of Physiology\, Anatomy and Genetics\, Univer sity of Oxford. “A role for the cortex in sleep-wake regulation”\n\n4: 50 – 5:10 Andrew Shelton (Packer & Butt Laboratories) Department of Phy siology\, Anatomy and Genetics\, University of Oxford. “The claustrum: F rom synapses to behaviour” \n\n5:10 – 5.30 Refreshments \n\nSPECIAL L ECTURE \n\n5:30 – 6:30 Matthew Larkum\, Humboldt University\, Berlin\, N eurocure Cluster of Excellence\, Neuroscience Research Center – Campus M itte\; Charité Universitätsmedizin Berlin “Coupling the state and cont ents of consciousness”\n\n6:30 – 7:00 Drinks reception with concluding remarks from Andrew King\n\nSpeakers:\n Various Speakers LOCATION:Sherrington Building (Small Lecture Theatre (second floor))\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/fe66c928-abdf-4024-9791-87eea2c1dd28/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Joint Meeting of Oxford Neuroscience & Neurocure Cluster of Excellence\, Charité Universitätsmedizin\, Berlin TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Mutual exclusive interactions between typical absence and limbic e pilepsy - Professor Filiz Onat (Department of Pharmacology and Clinical Ph armacology\, Marmara University School of Medicine\, Istanbul\, Turkey) DTSTART;VALUE=DATE-TIME:20191113T160000Z DTEND;VALUE=DATE-TIME:20191113T170000Z UID:https://talks.ox.ac.uk/talks/id/ee30f5b1-8466-43ed-9215-a1dc76be990d/ DESCRIPTION:It has been hypothesized that the mechanisms underlying limbic (focal) epilepsy are distinctively different from those responsible for t ypical absence (generalized) epilepsy and its seizures. Absence seizures\, which are typically associated with paroxysmal alterations in consciousne ss and 2.5-3 Hz spike-and-wave discharges in the EEG\, are the major clini cal manifestations of childhood and juvenile absence epilepsy. It has been suggested that the pathophysiology of absence seizures principally involv es a predominance of inhibitory activity in cortico-thalamo-cortical circu its. In contrast\, limbic seizures\, clinically seen as representative of mesial temporal lobe epilepsy\, have been shown to involve predominantly a n excessive cellular hyperexcitability in the limbic system\, with focal d ischarges in the EEG that can progress to secondary generalized convulsive seizures. In order to study the dissimilarities between limbic and genera lized typical absence epilepsy\, we developed a new paradigm in which we c ombined kindling as a limbic epilepsy model\, with genetic absence epileps y in rats.\nSpeakers:\nProfessor Filiz Onat (Department of Pharmacology an d Clinical Pharmacology\, Marmara University School of Medicine\, Istanbul \, Turkey) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/ee30f5b1-8466-43ed-9215-a1dc76be990d/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Mutual exclusive interactions between typical absence and limbic epilepsy - Professor Filiz Onat (Department of Pharmacology and Cl inical Pharmacology\, Marmara University School of Medicine\, Istanbul\, T urkey) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Schizophrenia as a disease of brain energy metabolism: The promise of therapeutic ketosis - Zoltán Sarnyai\, M.D\, Ph.D. (Lady Davis Visiti ng Professor\, Technion-Israel Institute of Technology\, Haifa\, Israel\, Professor of Pharmacology\, James Cook University\, Townsville\, Australia ) DTSTART;VALUE=DATE-TIME:20191017T140000 DTEND;VALUE=DATE-TIME:20191017T150000 UID:https://talks.ox.ac.uk/talks/id/994cd74d-f971-4dd2-91db-d3d7c9a67a40/ DESCRIPTION:Recent evidence suggest that there is a bioenergetics dysfunct ion characterized by abnormal glucose handling and mitochondrial deficit\, in the brain of people with schizophrenia. We identified that ketogenic d iet\, which provides alternative fuel to glucose for bioenergetic processe s in the brain\, normalises schizophrenia-like behaviours in translational ly relevant pharmacological\, genetic and neurodevelopmental mouse models. We have obtained preliminary evidence that the ketogenic substance beta-h ydroxybutyrate or faecal microbiota transfer from mice fed with ketogenic diet exert similar beneficial effects in mice maintained on standard diet. This talk will also provide some mechanistic insights on how ketogenic di et/ketosis may exert its therapeutic effect in schizophrenia.\n\nReference s:\n1. Sarnyai\, Z.\, Kraeuter\, A.K.\, Palmer\, C. Ketogenic diet for sch izophrenia: Clinical implication. Current Opinion in Psychiatry 2019 Sep\; 32(5):394-401.\n2. Kraeuter\, AK\, van den Buuse\, M.\, Sarnyai\, Z. Ketog enic diet and olanzapine treatment alone and in combination reduce a pharm acologically-induced prepulse inhibition deficit in female mice. Schizophr enia Research 2019 Aug 9. pii: S0920-9964(19)30344-5. doi: 10.1016/j.schre s.2019.08.002. [Epub ahead of print]\n3. Kraeuter\, AK\, van den Buuse\, M \, Sarnyai\, Z. Ketogenic diet prevents impaired prepulse inhibition of st artle in an acute NMDA receptor hypofunction model of schizophrenia. Schiz ophrenia Research 2019 Apr\;206:244-250. \n4. Kraeuter\, AK\, Loxton\, H.\ , Costa Lima\, B.\, Rudd\, D.\, Sarnyai\, Z. Ketogenic diet reverses behav ioral abnormalities in an acute NMDA receptor hypofunction model of schizo phrenia. Schizophrenia Res. 2015 Dec\;169(1-3):491-3.\n\nSpeakers:\nZoltá n Sarnyai\, M.D\, Ph.D. (Lady Davis Visiting Professor\, Technion-Israel I nstitute of Technology\, Haifa\, Israel\, Professor of Pharmacology\, Jame s Cook University\, Townsville\, Australia ) LOCATION:Sherrington Building (Large Lecture Theatre)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/994cd74d-f971-4dd2-91db-d3d7c9a67a40/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Schizophrenia as a disease of brain energy metabolism: Th e promise of therapeutic ketosis - Zoltán Sarnyai\, M.D\, Ph.D. (Lady Dav is Visiting Professor\, Technion-Israel Institute of Technology\, Haifa\, Israel\, Professor of Pharmacology\, James Cook University\, Townsville\, Australia ) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:SLM-based methods for 3D control and imaging in the brain - Darcy Peterka (Columbia University) DTSTART;VALUE=DATE-TIME:20190619T120000 DTEND;VALUE=DATE-TIME:20190619T130000 UID:https://talks.ox.ac.uk/talks/id/023da4cc-6766-4496-acd3-93a71792c2c3/ DESCRIPTION:Recording neuronal activity throughout the brain with high tem poral and spatial resolution may be a critical step in understanding how t he brain works. Task-based approaches allow intelligent trade-offs betwee n resolution\, speed\, and signal. I will describe projective two-photon i maging methods that leverage the spatiotemperal sparseness of neural activ ity and use holographic multiplexing and statistical source separation to create capable platforms for high performance imaging with single cell res olution. Similar holographic platforms can also be used to activate ensemb les of neurons with single cell precision\, and I will describe recent eff orts to improve targeting and control in awake behaving animals.\nSpeakers :\nDarcy Peterka (Columbia University) LOCATION:Sherrington Building (Small Lecture Theatre)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/023da4cc-6766-4496-acd3-93a71792c2c3/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:SLM-based methods for 3D control and imaging in the brain - Darcy Peterka (Columbia University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Music\, reward and clinical applications - Dr. Noèlia Martínez-M olina (Department of Psychology and Logopedics Faculty of Medicine\, Unive rsity of Helsinki) DTSTART;VALUE=DATE-TIME:20190528T160000 DTEND;VALUE=DATE-TIME:20190528T170000 UID:https://talks.ox.ac.uk/talks/id/c09d47f5-ae44-4c0e-a058-91b67ec19965/ DESCRIPTION:Abstract: Music is a highly complex\, multidomain stimulus tha t engages a large-scale bilateral network of brain areas associated with a uditory perception\; language and syntactic and semantic processing\, atte ntion and working memory\, semantic and episodic memory\, rhythmic and mot or functions\, and emotions and reward. Notably\, musical training can sha pe the structure and function of the brain thus driving clinical interest on the use of music-based interventions in neurological rehabilitation. In this talk\, I will introduce our findings on people with specific musical anhedonia\, i.e individuals who do not derive pleasure from music despite intact reward processing for other reinforcers. In particular\, I will pr esent structural and functional MRI results showing that i) there is a dis sociation in the activity of the reward system for musical pleasure and mo netary gains in this group of people\, ii) the white matter microstructure of the paths connecting the perceptual and reward systems is associated w ith individual differences in music reward sensitivity. Finally\, I will g ive an overview of a randomized controlled trial with traumatic brain inju ry patients using music therapy and its effects on executive functions\, b rain morphometry\, and resting-state functional connectivity. Overall\, th ese results add up to an increasing body of evidence for the capacity of m usic to engage widespread cognitive and emotional systems and to its effic acy in the rehabilitation of neurological disorders.\n\nShort bio: Dr. No èlia Martínez-Molina is a biologist and cognitive neuroscientist interes ted in understanding how the neural activity in emotion and reward process ing is modulated by music and in the use of music for rehabilitating cogni tive and emotional functioning in neurological disorders. She defended her PhD in Experimental Psychology from the University of Barcelona in 2017. This work integrated behavioural methods with structural and functional MR I to study the neural correlates of individuals with specific musical anhe donia\, i.e. showing a selective reduction in musical pleasure despite nor mal perceptual abilities and preserved reward-related response in other do mains. She is now a postdoctoral fellow with Dr. Teppo Särkämö in the M usic\, Ageing and Rehabilitation Team (MART) working on the analysis of lo ngitudinal neuroimaging data from traumatic brain injury and stroke patien ts with aphasia. \nSpeakers:\nDr. Noèlia Martínez-Molina (Department of Psychology and Logopedics Faculty of Medicine\, University of Helsinki) LOCATION:Sherrington Building (Small Lecture Theatre)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/c09d47f5-ae44-4c0e-a058-91b67ec19965/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Music\, reward and clinical applications - Dr. Noèlia Ma rtínez-Molina (Department of Psychology and Logopedics Faculty of Medicin e\, University of Helsinki) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Adhesion-dependent modulation of signalling in neural differentiat ion\, axon guidance and medulloblastoma - Professor Andrew Furley (Departm ent of Biomedical Science\, The University of Sheffield) DTSTART;VALUE=DATE-TIME:20190227T140000Z DTEND;VALUE=DATE-TIME:20190227T150000Z UID:https://talks.ox.ac.uk/talks/id/6c66c557-1e87-4a70-80d2-23b5736ff180/ DESCRIPTION:\nSpeakers:\nProfessor Andrew Furley (Department of Biomedical Science\, The University of Sheffield) LOCATION:Sherrington Building (Small Lecture Theatre)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/6c66c557-1e87-4a70-80d2-23b5736ff180/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Adhesion-dependent modulation of signalling in neural dif ferentiation\, axon guidance and medulloblastoma - Professor Andrew Furley (Department of Biomedical Science\, The University of Sheffield) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Mitochondrial dysfunction in neonatal brain injury - Dr Claire Tho rton (King’s College London.) DTSTART;VALUE=DATE-TIME:20190308T110000Z DTEND;VALUE=DATE-TIME:20190308T120000Z UID:https://talks.ox.ac.uk/talks/id/1e226e2f-b333-4c93-a583-671a044ca4b1/ DESCRIPTION:Neonatal hypoxic-ischaemia at term results in life-long conseq uences for those infants severely affected. The gold standard treatment\, therapeutic hypothermia\, provides proof-of-concept that post-injury inter vention can be effective. However hypothermia is not universally successfu l and there is an urgent need for synergistic therapies. Mitochondrial dys function lies at the centre of the development of neonatal brain injury fo llowing hypoxic-ischaemic insult. Not only is mitochondrial dysfunction ke y in triggering apoptotic cell death but in vivo studies of hypoxic-ischae mia in rodents and in vitro oxygen/glucose deprivation have identified per turbations in mitochondrial dynamics affecting fission\, fusion and mitoph agy. In particular\, the integrity of the mitochondrial fusion protein\, O ptic Atrophy (OPA)1 appears significantly vulnerable to such insult. Our c urrent research focusses on mechanisms underlying impaired mitochondrial f ission and fusion in order to develop strategies for maintaining mitochond rial function\, ultimately providing additional neuroprotection for infant s following birth asphyxia\, where therapeutic hypothermia alone is inadeq uate.\nSpeakers:\nDr Claire Thorton (King’s College London.) LOCATION:Sherrington Building (Small Lecture Theatre)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/1e226e2f-b333-4c93-a583-671a044ca4b1/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Mitochondrial dysfunction in neonatal brain injury - Dr C laire Thorton (King’s College London.) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Impact of neuroinflammation on brain development in premature infa nts - Pierre Gressens MD PhD (Inserm U1141 and Université Paris Diderot\, Paris & Centre for the Developing Brain\, KCL\, London) DTSTART;VALUE=DATE-TIME:20190402T130000 DTEND;VALUE=DATE-TIME:20190402T140000 UID:https://talks.ox.ac.uk/talks/id/6bcc5863-860e-4255-a80f-a4ceb9f8840b/ DESCRIPTION:Epidemiological studies have shown a strong association betwee n perinatal infection / inflammation and brain damage in the newborn and/o r neurological handicap in survivors. Experimental studies have allowed to show a causal effect of infection / inflammation on perinatal brain damag e. \n\nInfection / inflammatory factors can induce brain damage by themsel ves. Accordingly\, injection of E Coli to pregnant rabbits induces periven tricular white matter cysts and widespread white matter cell death\, mimic king brain damage observed in preterm infants. In addition\, injection of Ureaplasma Parvum to pregnant mice induces myelin defects and loss of inte rneurons in the offspring. Similarly\, injection of LPS to pregnant rats i nduces transient central inflammation and myelination defects in the offsp ring. \n\nAlternatively\, in the so-called multiple hit hypothesis\, infec tion / inflammation can act as predisposing factors making the brain more susceptible to a second stress (sensitization process). Indeed\, injection of low doses LPS to developing rats makes the newborn brain significantly more susceptible to hypoxic-ischemic insult. Similarly\, injection of int erleukin-1-beta to newborn mice or rats makes the brain much more sensitiv e to an excitotoxic insult. Current studies are evaluating the time window during which sensitization of the brain will persist after exposure to in flammatory factors in the perinatal period. In addition\, the mechanisms b y which sensitization is working are not yet fully undertsood but could in clude changes in gene transcription and modifications of glutamate recepto r activity. \n\nEpidemiological data also suggest that perinatal exposure to inflammatory factors could predispose to long term diseases including p sychiatric disorders. This could be particularly the case for preterm infa nts whose brain could be more sensitive to environmental factors when comp ared to full term infants. In this context\, exposure of newborn mice to l ow doses of interleukin-1-beta during the neonatal period has been recentl y shown to disrupt oligodendrocyte maturation\, myelin formation and axona l development. These white matetr abnormalities are moderate during the de velopmental period but do persist until adulthood. They lead to permanent deficiencies in behavioral tests without detectable effects on motor funct ions. The underlying molecular mechanisms include alterations of the trans cription of genes implicated in oligodendrogenesis\, myelin formation and axonal maturation. \n\nAltogether\, these clinical and experimental data s trongly support the hypothesis that exposure to infection / inflammation d uring pregnancy or the eprinatal period is deleterious for the brain. This can lead to the appearance of perinatal brain damage that can lead to lon g term neurological and cognitive disabilities. In addition\, some data al so suggest that the perinatal exposure to inflammatory factors can alter t he programs of brain development. \nSpeakers:\nPierre Gressens MD PhD (Ins erm U1141 and Université Paris Diderot\, Paris & Centre for the Developin g Brain\, KCL\, London) LOCATION:Sherrington Building (Small Lecture Theatre )\, off Parks Road OX 1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/6bcc5863-860e-4255-a80f-a4ceb9f8840b/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Impact of neuroinflammation on brain development in prema ture infants - Pierre Gressens MD PhD (Inserm U1141 and Université Paris Diderot\, Paris & Centre for the Developing Brain\, KCL\, London) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:CUBIC-HistoVIsion: a pipeline for three-dimensional whole-organ/bo dy staining and imaging with single-cell resolution based on chemical prop erties of tissue gel - Dr Etsuo A. Susaki (The University of Tokyo Graduat e School of Medicine) DTSTART;VALUE=DATE-TIME:20190307T140000Z DTEND;VALUE=DATE-TIME:20190307T150000Z UID:https://talks.ox.ac.uk/talks/id/82b23cfa-51b3-4eb9-8623-2f02b8c9dcf6/ DESCRIPTION:The recent development of various tissue clearing and three-di mensional (3D) imaging methods\, including our CUBIC technology\, enabled the comprehensive observation of whole organ/body with cellular resolution or more. Several studies tried to integrate whole-mount staining into the clearing-imaging scheme. However\, due to the difficulty in efficient pen etration of stains and antibodies\, they have only been applied in loose e mbryonic tissues or with a limited number of antibodies/stains for adult r odent tissues. To logically identify the critical parameters for the effic ient penetration\, we began by investigating material chemistry of fixed a nd delipidated biological tissue. Then\, we performed a surrogate assay wi th an artificial material similar to tissue in order to widely examine mul tiple parameters for efficient staining. The identified parameters were in tegrated as a general 3D staining protocol\, with which we have confirmed ~30 chemicals and antibodies used in whole adult mouse brain staining and imaging with single-cell resolution. The developed “CUBIC-HistoVIsion” pipeline for 3D histochemistry and volumetric imaging provides opportunit ies for multi-channel imaging of functional and structural molecules of wh ole adult mouse organs as well as primate organs\, thus will be widely app lied to life science and medical researches in future.\n\nSusaki et al. Ce ll 157: 726-739 2014.\nTainaka et al. Cell 159: 911-924\, 2014.\nSusaki et al. Nat Protocols 10: 1709-1727\, 2015.\nSusaki and Ueda. Cell Chemical B iology 23:137-157\, 2016. (Review)\nTatsuki et al. Neuron 90: 70-85\, 2016 .\nNojima et al. Sci Rep 7: 9269\, 2017.\nTainaka et al. Cell Rep 24: 2196 -2210.e9\, 2018.\nSusaki et al. in prep.\nSpeakers:\nDr Etsuo A. Susaki (T he University of Tokyo Graduate School of Medicine) LOCATION:Sherrington Building (Large Lecture Theatre)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/82b23cfa-51b3-4eb9-8623-2f02b8c9dcf6/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:CUBIC-HistoVIsion: a pipeline for three-dimensional whole -organ/body staining and imaging with single-cell resolution based on chem ical properties of tissue gel - Dr Etsuo A. Susaki (The University of Toky o Graduate School of Medicine) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Area-specific mapping of binocular disparity across mouse visual c ortex - Alessandro La Chioma (Max Planck Institute of Neurobiology\, Syna pses – Circuits – Plasticity\, Martinsried\, Germany) DTSTART;VALUE=DATE-TIME:20190211T160000Z DTEND;VALUE=DATE-TIME:20190211T170000Z UID:https://talks.ox.ac.uk/talks/id/613536b7-fa93-483d-8d24-2cfd54cbaa2d/ DESCRIPTION:Mouse visual cortex is a complex network comprising the primar y visual cortex (V1) and several higher- order visual areas. Although thes e visual cortical areas are believed to contribute differentially to perce ption and behavior\, our understanding of their role in visual processing is still unclear.\n\nMouse V1\, along with the higher visual areas LM and RL\, contains a substantial visuotopic representation of the binocular fie ld of view. Binocular neurons in the visual cortex combine signals from le ft and right eye images. The small differences between these images\, call ed binocular disparities\, provide the visual system with critical informa tion for depth perception. In primates\, disparity selectivity is differen tially processed across visual cortical areas. To test whether such specia lizations also exist in rodents\, we characterized binocular disparity in V1 and in areas LM and RL of the anesthetized mouse. We employed a dichopt ic stimulation protocol\, using oriented gratings presented at varying int erocular phases as well as random dot stereograms.\n\nWe found that dispar ity processing is highly distributed across neurons in areas V1\, LM\, and RL\, but with clear differences in preferred disparities: area RL contain s a higher fraction of neurons selective to near disparities compared to V 1 and LM\, indicating that RL is specialized for processing visual objects at close distance to the mouse. Preference for near disparities in RL was evident using both gratings and random dot stereograms for stimulation\, and it was also observed in awake animals. Since recent data show that mos t neurons in mouse RL respond to both visual and whisker stimulation\, we speculate that this area might contain a multimodal representation of the immediate space in front of the animal.\nSpeakers:\nAlessandro La Chioma ( Max Planck Institute of Neurobiology\, Synapses – Circuits – Plasticit y\, Martinsried\, Germany) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/613536b7-fa93-483d-8d24-2cfd54cbaa2d/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Area-specific mapping of binocular disparity across mouse visual cortex - Alessandro La Chioma (Max Planck Institute of Neurobiolo gy\, Synapses – Circuits – Plasticity\, Martinsried\, Germany) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Using zebrafish to study myelinated axons in vivo - Professor Davi d Lyons (Centre for Discovery Brain Sciences\, The University of Edinburgh ) DTSTART;VALUE=DATE-TIME:20190123T160000Z DTEND;VALUE=DATE-TIME:20190123T170000Z UID:https://talks.ox.ac.uk/talks/id/cbee700b-2c75-48e1-9c9b-27cff08f3823/ DESCRIPTION:Myelinated axons comprise about half the volume of our central nervous system and are essential to its formation\, function\, and life-l ong health. Work over the past decade has established the zebrafish as a v aluable model for the study of myelinated axons. The embryos and larvae of zebrafish have fantastic properties for live cell imaging in vivo. Their small size\, rapid development and optical transparency\, coupled with the availability of numerous fluorescent reporters\, allow visualisation of c ellular and molecular behaviours in vivo in ways that are not possible in other systems. I will give an overview of the tools that we have developed in my laboratory to study myelinated axons in vivo\, and focus on our rec ent work investigating how axon-oligodendrocyte interactions regulate the dynamics of myelination in the CNS. Zebrafish are also amenable to large-s cale genetic and chemical screens\, and I will provide an update on novel insights gained into myelin formation\, and maintenance through such scree ns.\n\nIn addition\, I will also describe our recent establishment of a fu lly automated high-resolution chemical screening platform for the identifi cation of compounds that may be employed to promote myelin regeneration an d the treatment of disease. Finally\, I will outline our burgeoning effort s to assess how the dynamic regulation of myelination by neural activity a ffects fundamental principles of circuit function.\nSpeakers:\nProfessor D avid Lyons (Centre for Discovery Brain Sciences\, The University of Edinbu rgh) LOCATION:Le Gros Clark Building (Large Lecture Theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/cbee700b-2c75-48e1-9c9b-27cff08f3823/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Using zebrafish to study myelinated axons in vivo - Profe ssor David Lyons (Centre for Discovery Brain Sciences\, The University of Edinburgh) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Development of the human insula - Professor Gundela Meyer (Departm ent of Anatomy\, Pathological Anatomy and Histology Universidad de La Lagu na ULL) DTSTART;VALUE=DATE-TIME:20181207T130000Z DTEND;VALUE=DATE-TIME:20181207T140000Z UID:https://talks.ox.ac.uk/talks/id/96df227b-0b32-4ee7-adb9-2dd596dd0671/ DESCRIPTION:The human insula is a key node in a neuronal network which int egrates interoceptive stimuli from the own body\, and exteroceptive stimul i from the environment\, and thus maintains the autonomic\, emotional and socio-cognitive homeostasis of the body. In the last years\, the insula ha s come into the focus of attention. Comparative anatomical studies showed that in many species the insula forms the lateral edge of the cortex. Very little is known about the prenatal development of the human insula\, whic h is the first cortical region to mature. The origin of the pyramidal neur ons for the insula is in a small sector of the proliferating ventricular/s ubventricular zone at the cortico-striatal boundary (CSB). The CSB contain s the radial glia cells\, which are stem cells and give rise to a dense fa scicle of radial glia processes. This fascicle traverses the external caps ule and serves as a migration substrate for the neuroblasts on their way f rom the CSB into the insula. Around the 10/11th week of gestation\, the la teral ventricle and its adjacent structures including the CSB bend in a C- shaped fashion. The insula now develops between a dorsal\, fronto-parietal and a ventral\, temporal CSB\, which provide descending and ascending str eams of neuroblasts\, respectively\, migrating along the radial glia fasci cle. As a consequence of the ventricular rotation during ontogenesis\, the human insula changes its initial position at the lateral edge of the cort ex to its final central location\, which reflects its integrative function s in brain activity.\nSpeakers:\nProfessor Gundela Meyer (Department of An atomy\, Pathological Anatomy and Histology Universidad de La Laguna ULL) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/96df227b-0b32-4ee7-adb9-2dd596dd0671/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Development of the human insula - Professor Gundela Meyer (Department of Anatomy\, Pathological Anatomy and Histology Universidad d e La Laguna ULL) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:“Artiphysiology” reveals V4-like shape tuning in a deep networ k trained for image classification - Prof Wyeth Bair (University of Washin gton) DTSTART;VALUE=DATE-TIME:20180823T150000 DTEND;VALUE=DATE-TIME:20180823T160000 UID:https://talks.ox.ac.uk/talks/id/02ca0f9b-da64-41bc-818d-13215bf6e7a9/ DESCRIPTION:Deep convolutional neural networks (CNNs) provide a potentiall y rich source of insight for understanding mid-level visual processing in the primate cerebral cortex. Taking the approach of an electrophysiologist to characterizing single CNN units\, we found that many units exhibit tra nslation-invariant boundary curvature selectivity approaching that of the best neurons in the mid-level visual area V4. \nFor some of these V4-like units\, particularly in the middle layers\, the natural images that drove them best were also qualitatively consistent with selectivity for object b oundaries. Our results identify a novel image-computable model for V4 boun dary curvature selectivity and suggest that such a representation may begi n to emerge within the middle layers of an artificial network trained for image categorization\, even though boundary information was not provided d uring training. This raises the general possibility that single-unit featu re selectivity learned in CNNs may become a valuable guide for understandi ng sensory cortex.\nSpeakers:\nProf Wyeth Bair (University of Washington) LOCATION:Sherrington Library\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/02ca0f9b-da64-41bc-818d-13215bf6e7a9/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:“Artiphysiology” reveals V4-like shape tuning in a de ep network trained for image classification - Prof Wyeth Bair (University of Washington) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Early Neuronal Diversity Shapes Cortical Circuit Assembly - Dr Lyn ette Lim (MCR Centre for Developmental Neurobiology\, King's College Londo n) DTSTART;VALUE=DATE-TIME:20180626T110000 DTEND;VALUE=DATE-TIME:20180626T120000 UID:https://talks.ox.ac.uk/talks/id/103539e6-4362-4fd5-945c-d3d6d81cdc6b/ DESCRIPTION:Neural circuit assembly relies on the precise synchronisation of developmental processes such as cell migration and axon targeting\, but the cell autonomous mechanisms coordinating these events remain largely u nknown. We found that different classes of interneurons use distinct route s of migration to reach the embryonic cerebral cortex. Somatostatin-expres sing interneurons that migrate through the marginal zone develop into Mart inotti cells\, one of the most distinctive class of cortical interneurons. For these cells\, migration through the marginal zone is linked to the de velopment of their characteristic layer 1 axonal arborization. Alteration of the normal migratory route of Martinotti cells by conditional deletion of Mafb – a gene that is preferentially expressed by these cells – cel l-autonomously disrupts axonal development and impairs the function of the se cells in vivo. Our results suggest that migration and axon targeting pr ograms are coupled to optimize the assembly of inhibitory circuits in the cerebral cortex.\nSpeakers:\nDr Lynette Lim (MCR Centre for Developmental Neurobiology\, King's College London) LOCATION:Sherrington Building (Library)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/103539e6-4362-4fd5-945c-d3d6d81cdc6b/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Early Neuronal Diversity Shapes Cortical Circuit Assembly - Dr Lynette Lim (MCR Centre for Developmental Neurobiology\, King's Coll ege London) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Structural Basis for Centrifugal Regulation of the Olfactory Bulb ~individual labeling and correlated Laser and volume/high-voltage EM micro scopies~ - Professor Kazunori Toida MD\, PhD (Kawasaki Medical School) DTSTART;VALUE=DATE-TIME:20180619T160000 DTEND;VALUE=DATE-TIME:20180619T170000 UID:https://talks.ox.ac.uk/talks/id/be9798f6-3712-4755-8ee8-dfe5e7e87321/ DESCRIPTION:Olfaction has been revealed as an attractive system in the bra in by recent molecular biological and physiological studies using function al recording\, which indicated elaborate mechanisms for processing olfacto ry information in the main olfactory bulb. Modern advanced technologies ha ve enabled us to label bulbar neurons selectively\, and even individually. Thus I can show how the rodent olfactory bulb is regulated centrifugally by serotonergic\, cholinergic and noradrenergic projections\, as well as i ntrinsically by estradiol with an enormous amount of findings collected fr om directly correlated laser scanning microscopy\, digital wide-field volu me electron microscopy\, ultra-high voltage electron microscopy\, and elec tron tomography. Current uncertainties and issues that need to be clarifie d in the future are also discussed.\n\nToida K. 2008\, Kiyokage et al 2010 \, Suzuki et al 2015\, Hamamoto et al 2016\, Kiyokage et al 2017\, Matsuno et al 2017 http://www.uhvem.osaka-u.ac.jp/\n\nFor more information:zoltan .molnar@dpag.ox.ac.uk\; shuichi.hayashi@dpag.ox.ac.uk\n\nSpeakers:\nProfes sor Kazunori Toida MD\, PhD (Kawasaki Medical School) LOCATION:Le Gros Clark Building (Large Lecture Theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/be9798f6-3712-4755-8ee8-dfe5e7e87321/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Structural Basis for Centrifugal Regulation of the Olfact ory Bulb ~individual labeling and correlated Laser and volume/high-voltage EM microscopies~ - Professor Kazunori Toida MD\, PhD (Kawasaki Medical Sc hool) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Cortical integration from V1 into V4 along the object-processing h ierarchy - Professor Wei Wang (Institute of Neuroscience\, Shanghai) DTSTART;VALUE=DATE-TIME:20180618T154500 DTEND;VALUE=DATE-TIME:20180618T164500 UID:https://talks.ox.ac.uk/talks/id/fc2f69e6-0cd5-436a-9885-705e578988e0/ DESCRIPTION:Human and non‐human primates effortlessly see both global an d local features of objects in great detail. However\, how the cortex inte grates local visual cues to form global representations along visual hiera rchies remains mysterious\, particularly considering a long-standing parad ox in vision as neurally encoded complexity increases along the visual hie rarchy\, the known acuity or resolving power dramatically decreases. Putti ng it simply\, how do we simultaneously recognize the face of our child\, while still resolving the individual hairs of her or his eyelashes? Many m odels of visual processing follow the idea that low-level resolution and p osition information is discarded to yield high-level representations (incl uding cutting-edge deep learning models). These are themes that are fundam ental to conceiving how the brain does sensory transformation! \n\nCombini ng large-scale imaging of high spatial resolution to record the transforma tion of information across three visual areas simultaneously (V1\, V2\, an d V4) with electrophysiological multi-site laminar recordings\, we found a bottom-up cascade of cortical integration of local visual cues as general cortical mechanisms for global representations in primate ventral and dor sal streams. The integrated neural responses are dependent on the sizes an d preferences of their receptive fields. Recently\, we reveal an unexpecte d neural clustering preserving visual acuity from V1 into V4\, enabling a detailed spatiotemporal separation of local and global features along the object-processing hierarchy\, suggesting that higher acuities are retained to later stages where more detailed cognitive behaviour occurs. The study reinforces the point that neurons in V4 (and most likely also in infero-t emporal cortex) do not necessarily need to have only low visual acuity\, w hich may begin to resolve the long-standing paradox concerning fine visual discrimination. Thus\, our research will prompt further studies to probe how preservation of low-level information is useful for higher-level visio n and provide new ideas to inspire the next generation of deep neural netw ork architectures.\nSpeakers:\nProfessor Wei Wang (Institute of Neuroscien ce\, Shanghai) LOCATION:Sherrington Building (Sherrington Library)\, off Parks Road OX1 3 PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/fc2f69e6-0cd5-436a-9885-705e578988e0/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Cortical integration from V1 into V4 along the object-pro cessing hierarchy - Professor Wei Wang (Institute of Neuroscience\, Shangh ai) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:DEVELOPMENTAL LINK BETWEEN FETAL AND ADULT LEYDIG CELLS - Yuichi S hima MD PhD (Kawasaki Medical School\, Japan) DTSTART;VALUE=DATE-TIME:20180619T160000 DTEND;VALUE=DATE-TIME:20180619T164500 UID:https://talks.ox.ac.uk/talks/id/8e904467-9004-45d5-b0ff-0435f5dd9afd/ DESCRIPTION:\nStatus: This talk has been cancelled\nTesticular Leydig cell s induce masculinization of the whole body by producing androgens. It is w ell accepted that two distinct Leydig cell populations\, fetal Leydig cell s (FLCs) and adult Leydig cells (ALCs)\, develop in the prenatal and postn atal stages\, respectively. In case of mice\, FLCs appear at around E12.5 and increase in number during fetal stages. The number of FLCs decreases a fter birth\, and thereafter ALCs appear and increase in number rapidly dur ing puberty. Although both FLCs and ALCs produce androgens\, lineage relat ionship between FLCs and ALCs was unclear\, and it remained an open questi on how two distinct Leydig cell populations sequentially differentiate in the testicular interstitium.\nAd4BP/SF-1 (Ad4-binding protein/Steroidogeni c factor-1\, officially NR5A1) is a nuclear receptor expressed in both FLC s and ALCs. We revealed that an upstream enhancer of Ad4BP/SF-1 gene has a potential to induce gene expression in FLCs but not ALCs. Therefore\, we designated this enhancer as Fetal Leydig Enhancer (FLE) of Ad4BP/SF-1 gene . We performed lineage tracing of FLCs by using FLE and revealed that a pa rt of FLCs dedifferentiate around birth and redifferentiate to ALCs at pub ertal stage. Moreover\, the dedifferentiated cells contribute to the perit ubular myoid cells (PTMCs) and vascular pericytes (VPs) in the testicular interstitium. Although steroidgenic gene expression is completely absent i n the PTMCs and VPs\, they retained a potential to redifferentiate into AL Cs at pubertal stage\, suggesting that they serve as potential ALC stem ce lls. Given the functional importance of Ad4BP/SF-1 in Leydig cell differen tiation\, two distinct mouse models\, FLC lineage specific Ad4BP/SF-1 gene disrupted mice and the mice lacking fetal Leydig enhancer (FLE) of Ad4BP/ SF-1 gene\, were generated. Both mouse lines demonstrated closely similar phenotypes\; almost complete loss of FLCs\, conspicuous decline or complet e loss of ALCs\, and massive interstitial fibrosis. These results support the conclusion that FLC and ALC sequentially arise from a single lineage\, and FLE of Ad4BP/SF-1 gene is essential for not only initial FLC differen tiation but also pubertal ALC redifferentiation.\n\nFor more information: zoltan.molnar@dpag.ox.ac.uk\; shuichi.hayashi@dpag.ox.ac.uk\n\nSpeakers:\n Yuichi Shima MD PhD (Kawasaki Medical School\, Japan) LOCATION:Le Gros Clark Building (Large Lecture Theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/8e904467-9004-45d5-b0ff-0435f5dd9afd/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:DEVELOPMENTAL LINK BETWEEN FETAL AND ADULT LEYDIG CELLS - Yuichi Shima MD PhD (Kawasaki Medical School\, Japan) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Pavlov in America: The influence of Pavlov on Lashley and Hebb - P rof Richard Brown (Dalhousie University) DTSTART;VALUE=DATE-TIME:20180531T160000 DTEND;VALUE=DATE-TIME:20180531T170000 UID:https://talks.ox.ac.uk/talks/id/b0d8b303-aecc-4b99-a395-6784e65e2345/ DESCRIPTION:Ivan P. Pavlov was awarded the Nobel Prize for Physiology or M edicine in December\, 1904 "in recognition of his work on the physiology o f digestion". By this time Pavlov had started to study "conditioned reflex es" and described how he came to study "psychical reflexes" in his "Madrid speech" (April 1903). In 1906\, Pavlov [spelled Pawlow] gave the Huxley L ecture\, entitled "The scientific investigation of the psychical faculties or processes in the higher animals" which was published in The Lancet (6 Oct. 1906). One of the earliest American proponents of classical condition ing was John B. Watson\, the founder of "Behaviorism". Watson conducted e xperiments on conditioned motor reflexes using the method of Bechterev and conducted his most infamous experiment on "Conditioned emotional reaction s" on "little Albert" in 1920. Karl S. Lashley did early work on condition ed salivary reflexes in humans. Pavlov visited America in 1923 and 1929 an d his Lectures on conditioned reflexes were published in English in 1927 a nd 1928. Pavlov provided American psychologists with an objective philosop hical approach as opposed to subjective methods such as introspection\; an d a methodological approach through the use of conditioned reflexes. Whil e these were embraced by Americans\, the theoretical approach to the study of higher nervous activity through conditioned reflexes\, was not so read ily embraced. Although Pavlov's methods of conditioned reflexes influenced the theories of Edwin Guthrie\, B.F. Skinner\, Clark Hull and Kenneth Spe nce\, Guthrie and Lashley (1930) were critical of Pavlov's theory of neura l function. Pavlov wrote a scathing reply to these critiques (1932). \n P avlov's student\, Boris Babkin influenced Donald Hebb to study conditioned reflexes and Hebb went on to develop a neurophysiological theory that i ntegrated the ideas of Pavlov and Sherrington on reflexes with the theorie s of Lashley\, Kohler and Tolman into a coherent theory that provided a ne ural mechanism that explained perception\, attention\, learning and memory . Hebb developed three ideas to provide a "modern" view of the neural chan ges underlying cognitive function: (1) the "Hebb synapse" or "Hebb learnin g rule"\; (2) the cell assembly and (3) the phase sequence.\n Today Pavlov ian conditioning is used to study the neurobiology of learning and memory at four levels: (1) behavioural\; (2) neural systems and circuits\; (3) ce llular mechanisms of synaptic plasticity\; and (4) molecular mechanisms of neural plasticity underlying learning and memory. Of note are the work of LeDoux\, Faneslow and others on the neural circuits of conditioned fear a nd the work of Thompson on the role of the cerebellum in conditioned motor responses. Pavlovian conditioning is also used to understand abnormal beh aviour and to develop clinical methods of behaviour therapy. Thus\, much o f the history of Psychology and Neuroscience in America has been influence d by the concepts of classical conditioning as developed by Pavlov\, criti cized by Lashley and incorporated into Hebb's neurophysiological theory.\n Speakers:\nProf Richard Brown (Dalhousie University) LOCATION:Le Gros Clark Building (Large Lecture Theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/b0d8b303-aecc-4b99-a395-6784e65e2345/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Pavlov in America: The influence of Pavlov on Lashley and Hebb - Prof Richard Brown (Dalhousie University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Understanding and reversing pathophysiological changes in Spinocer ebellar ataxia type 6 (SCA6) - Associate Professor Alanna Watt\, PhD (McGi ll University) DTSTART;VALUE=DATE-TIME:20180530T160000 DTEND;VALUE=DATE-TIME:20180530T170000 UID:https://talks.ox.ac.uk/talks/id/12544556-05ca-412c-af48-1138df50d840/ DESCRIPTION:\nSpeakers:\nAssociate Professor Alanna Watt\, PhD (McGill Uni versity) LOCATION:Sherrington Building (OCGF Seminar Room)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/12544556-05ca-412c-af48-1138df50d840/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Understanding and reversing pathophysiological changes in Spinocerebellar ataxia type 6 (SCA6) - Associate Professor Alanna Watt\, PhD (McGill University) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:"I wasn't going to eat it\, I was just going to taste it". Roles f or striatal plasticity in overeating and obesity. - Dr Carrie Ferrario (De partment of Pharmacology\, University of Michigan) DTSTART;VALUE=DATE-TIME:20180521T110000 DTEND;VALUE=DATE-TIME:20180521T120000 UID:https://talks.ox.ac.uk/talks/id/8faf9ba6-3fdd-4dbb-b8a9-9c328056bcbd/ DESCRIPTION:\nSpeakers:\nDr Carrie Ferrario (Department of Pharmacology\, University of Michigan) LOCATION:Sherrington Building (Small Lecture Theatre)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/8faf9ba6-3fdd-4dbb-b8a9-9c328056bcbd/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:"I wasn't going to eat it\, I was just going to taste it" . Roles for striatal plasticity in overeating and obesity. - Dr Carrie Fer rario (Department of Pharmacology\, University of Michigan) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Mechanisms Generating Cell-Type Diversity in Cerebral Cortex - Sim on Hippenmeyer\, PhD (Institute of Science and Technology Austria) DTSTART;VALUE=DATE-TIME:20180625T160000 DTEND;VALUE=DATE-TIME:20180625T170000 UID:https://talks.ox.ac.uk/talks/id/0472db1f-8e0b-47d0-8709-c854ebfe17d6/ DESCRIPTION:The concerted production of the correct number and diversity o f neurons and glia is essential for intricate neural circuit assembly. In the developing cerebral cortex\, radial glia progenitors (RGPs) are respon sible for producing all neocortical neurons and certain glia lineages. We recently performed a quantitative clonal analysis by exploiting the unprec edented resolution of the genetic MADM (Mosaic Analysis with Double Marker s) technology and discovered a high degree of non-stochasticity and thus d eterministic mode of RGP behavior. However\, the cellular and molecular me chanisms controlling the precise pre-programmed RGP lineage progression th rough proliferation\, neurogenesis and gliogenesis remain unknown. To this end we use quantitative MADM-based experimental paradigms at single RGP r esolution to define the non-cell-autonomous mechanisms and intrinsic funct ions of candidate genes controlling RGP-mediated cortical neuron and glia genesis and postnatal stem cell behavior.\n\nFor more information: zoltan. molnar@dpag.ox.ac.uk or noemi.picco@sjc.ox.ac.uk\nSpeakers:\nSimon Hippenm eyer\, PhD (Institute of Science and Technology Austria) LOCATION:Le Gros Clark Building (Large Lecture Theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/0472db1f-8e0b-47d0-8709-c854ebfe17d6/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Mechanisms Generating Cell-Type Diversity in Cerebral Cor tex - Simon Hippenmeyer\, PhD (Institute of Science and Technology Austria ) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Studying the function and connectivity of neural networks in zebra fish brain - Professor Emre Yaksi (Kavli Institute for Systems Neuroscienc e\, Norway) DTSTART;VALUE=DATE-TIME:20180416T160000 DTEND;VALUE=DATE-TIME:20180416T170000 UID:https://talks.ox.ac.uk/talks/id/76166b11-d76f-40d8-ad6c-bbd783bb25e0/ DESCRIPTION:The habenula (Hb) is a brain region with increasing popularity due to its strong link to addiction\, mood disorders and experience depen dent fear. We demonstrated that Hb neurons respond to odors and light asym metrically. Moreover\, we showed that Hb neurons exhibit structured sponta neous activity that is spatially and temporally organized. This spontaneou s activity resembles neural attractors\, which can switch the preferred st ate of the Hb and regulate the transmission of sensory information to down stream monoaminergic brainstem nuclei. In order to explore the source of H b spontaneous activity\, we investigate the local connectivity within Hb a nd the global functional inputs to Hb. Our results showed that recurrent e xcitatory con­nections within Hb is important for maintaining spatio-temp oral organization of Hb activity. Moreover\, we observed that functional i nputs form zebrafish homo­logues of hippocampus (Dl) and amygdala (Dm) an d sensory inputs from visual and olfactory systems are the major drivers o f spontaneous Hb activity. Our results suggested that these limbic and sen sory inputs are integrated in Hb in a non-linear fashion and can regulate sensory representations in Hb. We propose that Hb lies in the heart of a b rain wide network and act as “a hub” or “a switchboard”\, which ca n regulate or gate the communication of sensory systems and limbic forebra in areas with the monoaminergic brainstem nuclei that control animal behav iors.\nSpeakers:\nProfessor Emre Yaksi (Kavli Institute for Systems Neuros cience\, Norway) LOCATION:Le Gros Clark Building (Large Lecture Theatre )\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/76166b11-d76f-40d8-ad6c-bbd783bb25e0/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Studying the function and connectivity of neural networks in zebrafish brain - Professor Emre Yaksi (Kavli Institute for Systems Ne uroscience\, Norway) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Forebrain development in health and disease - Professor David Pric e (University of Edinburgh) DTSTART;VALUE=DATE-TIME:20180316T150000Z DTEND;VALUE=DATE-TIME:20180316T160000Z UID:https://talks.ox.ac.uk/talks/id/c2f32ba5-69b4-4a8e-af0d-0ed4c84ac3ad/ DESCRIPTION:\nSpeakers:\nProfessor David Price (University of Edinburgh) LOCATION:Le Gros Clark Building (Large Lecture Theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/c2f32ba5-69b4-4a8e-af0d-0ed4c84ac3ad/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Forebrain development in health and disease - Professor D avid Price (University of Edinburgh) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Deciphering SP8 regulative network for cortical development - Ugo Borello (University of Lyon) DTSTART;VALUE=DATE-TIME:20180316T160000Z DTEND;VALUE=DATE-TIME:20180316T170000Z UID:https://talks.ox.ac.uk/talks/id/70486aee-98f4-4afd-a72e-6dd7282cfb2f/ DESCRIPTION:The transcriptional network regulating forebrain development r emains relatively unknown. Molecules secreted by the different forebrain s ignaling centers establish the expression gradients of specific transcript ional factors\, which are necessary for the patterning and differentiation of the distinct structural and functional domains of the cerebral cortex. \nTo get new insights into the transcriptional regulation of forebrain de velopment we focused on the role of SP8\, a zinc finger transcription fact or involved in early patterning and arealization of the cortex. \nGenome w ide analysis of the SP8 binding sites and genetic manipulation of SP8 expr ession in the developing pallium allowed us to identify for the first time SP8 direct target genes\, and to determine a novel role for SP8 as a key transcriptional regulator of the first wave of cortical neurons differenti ation.\n\nSpeakers:\nUgo Borello (University of Lyon) LOCATION:Le Gros Clark Building (Large Lecture Theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/70486aee-98f4-4afd-a72e-6dd7282cfb2f/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Deciphering SP8 regulative network for cortical developme nt - Ugo Borello (University of Lyon) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:The role of extracellular vesicles in neurodegenerative diseases. - Professor Andrew Hill (La Trobe Institute for Molecular Science) DTSTART;VALUE=DATE-TIME:20170925T130000 DTEND;VALUE=DATE-TIME:20170925T140000 UID:https://talks.ox.ac.uk/talks/id/e7df7a15-c11f-492a-895c-57294f273424/ DESCRIPTION:Neurodegenerative disorders such as Alzheimer’s (AD)\, Parki nson’s (PD) and prion diseases are associated with proteins that misfold and deposit in the brain. Many cell types\, including neurons\, release e xtracellular vesicles (EVs) which include microvesicles and exosomes. EVs have been shown to be involved in processing of proteins such as APP\, α- synuclein\, and PrP which are those involved in AD\, PD and prion diseases respectively. Roles for these vesicles include cell-cell signalling\, rem oval of unwanted proteins\, and transfer of pathogens (including prion-lik e misfolded proteins) between cells. Our group has shown that EV’s conta in distinct processed forms of these proteins and that\, in the case of pr ion disease\, they contain the transmissible form of the misfolded protein . In addition to their protein content these vesicles have recently been s hown to contain genetic material in the form of protein coding (mRNA) and noncoding RNA species. We have analysed the protein and genetic cargo of E Vs from a number of cell types and using deep sequencing\, characterised t he RNA cargo of these vesicles. As exosomes can be isolated from circulati ng fluids such as serum\, urine\, and cerebrospinal fluid (CSF)\, they pro vide a potential source of biomarkers for neurological conditions. This ta lk will review the roles these vesicles play in neurodegenerative disease and highlight their potential in diagnosing these disorders through analys is of their RNA content.\nSpeakers:\nProfessor Andrew Hill (La Trobe Insti tute for Molecular Science) LOCATION:Le Gros Clark Building (Small lecture theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/e7df7a15-c11f-492a-895c-57294f273424/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:The role of extracellular vesicles in neurodegenerative d iseases. - Professor Andrew Hill (La Trobe Institute for Molecular Science ) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Out of Africa\, there is always something new – the unusual brai ns of some African mammals - Paul Manger PhD (Professor\, School of Anatom ical Sciences\, University of the) DTSTART;VALUE=DATE-TIME:20171003T160000 DTEND;VALUE=DATE-TIME:20171003T170000 UID:https://talks.ox.ac.uk/talks/id/da34a697-25f1-4775-87c8-cac5235475ec/ DESCRIPTION:Pliny the Elder is quoted as saying that something new always arises from Africa\, but he wasn't\nprophetically referring to the brains of African mammals. Africa is home to 25% of all extant mammal\nspecies\, all belonging to the Eutherian\, or placental\, mammals\, which includes h umans. Mammalian\nspecies indigenous to Africa have representatives in mos t major Eutherian mammal phylogenetic\norders\, and range from mammals as small as the pygmy mouse through to the largest terrestrial\nmammal the Af rican elephant. This talk will present the more unusual neuroanatomical\, neurochemical\nand sleep findings we have made in my laboratory over the p ast 15 years. We have been fortunate\nenough to study the brains of iconic mammal species\, such as the African elephant\, zebras\, lions and\ngiraf fe\, and many lesser-known species such as pangolins\, mole rats\, springh ares\, golden moles\, bats\nand hyraxes. While the work has focussed upon the nuclei of the brain that control the sleep-wake\ncycle\, observations made in other systems of the brain are also of broad interest. The potenti al\nsignificance of these findings and their relationships to understandin g the evolutionary plasticity of the\nbrain and behaviour\, and understand ing brain function in relation to behaviour more generally\, will be\npres ented on a case-by-case basis.\nSpeakers:\nPaul Manger PhD (Professor\, Sc hool of Anatomical Sciences\, University of the) LOCATION:Le Gros Clark Building (Large Lecture Theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/da34a697-25f1-4775-87c8-cac5235475ec/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Out of Africa\, there is always something new – the unu sual brains of some African mammals - Paul Manger PhD (Professor\, School of Anatomical Sciences\, University of the) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:There and back again: corticothalamic modulation of cortical sound processing - Dr Daniel Pooley (Eaton-Peabody Laboratories\, Massachusetts Eye and Ear Infirmary\, Boston\, MA 02114\, USA\; Department of Otolaryng ology\, Harvard Medical School\, Boston\, MA 02114\, USA.) DTSTART;VALUE=DATE-TIME:20160614T160000 DTEND;VALUE=DATE-TIME:20160614T170000 UID:https://talks.ox.ac.uk/talks/id/9c54e026-da60-4a24-b6f1-36d696cc9519/ DESCRIPTION:Beginning with the descriptions of Ramon y Cajal over a centur y ago\, anatomists have noted the massive projection from deep layers of s ensory cortex to the thalamus. A functional role for these corticothalamic connections has proven harder to define. Recent work in the primary visua l cortex has shown that layer 6 corticothalamic neurons (L6CT) dynamically adjust the gain on cortical sensory processing by engaging local networks of fast-spiking (FS) interneurons. I will present new evidence that L6CT neurons in the mouse auditory cortex can bi-directionally control the gain on cortical and thalamic sensory processing by entraining the phase of lo w-frequency cortical oscillations. The underlying circuit appears to share several features in common with the visual cortex\, including a central r ole for FS interneurons\, though there are also several key differences. T he neurophysiological dynamics translate directly to sound perception as L 6CT activation can bias the mouse towards heightened detection of faint so unds at the expense of accurate frequency discrimination\, or vice versa\, depending solely on the relative timing between the sensory trace and L6C T activity. These findings may have interesting implications for the neur al underpinnings of adaptive sensory processing.\nSpeakers:\nDr Daniel Poo ley (Eaton-Peabody Laboratories\, Massachusetts Eye and Ear Infirmary\, Bo ston\, MA 02114\, USA\; Department of Otolaryngology\, Harvard Medical Sch ool\, Boston\, MA 02114\, USA.) LOCATION:Sherrington Building (The Library\, Sherrington Building\, Depart ment of Physiology\, Anatomy and Genetics)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/9c54e026-da60-4a24-b6f1-36d696cc9519/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:There and back again: corticothalamic modulation of corti cal sound processing - Dr Daniel Pooley (Eaton-Peabody Laboratories\, Mass achusetts Eye and Ear Infirmary\, Boston\, MA 02114\, USA\; Department of Otolaryngology\, Harvard Medical School\, Boston\, MA 02114\, USA.) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Mouse Talk: The applications of neurobiological models of mammalia n hearing to the classification of mouse vocalizations - Associate Profess or Neil McLachlan (Melbourne School of Psychological Sciences\, University of Melbourne) DTSTART;VALUE=DATE-TIME:20151113T160000Z DTEND;VALUE=DATE-TIME:20151113T170000Z UID:https://talks.ox.ac.uk/talks/id/fa1f4217-dc0f-4e37-9d6b-4f06ddebc139/ DESCRIPTION:Extensive auditory neuroscience research that has focussed on the primary auditory pathways has failed to explain basic auditory functio ns such as sound recognition\, auditory object streaming and habituation. Extra lemniscal auditory pathways including the ponto-cerebellar networks are well documented\, and their involvement in conditioned reflexes in ani mals has even been computational modelled. In this talk I propose that con ditioned reflexes are a primitive form of sound recognition (with a motor output)\, and so sound recognition more generally would likely recruit thi s evolutionarily ancient neurobiological pathway. I will present a pathway model of auditory processing in the ponto-cerebellar pathways in humans a nd animals\, and its interconnections with emotion processing in the limbi c system and higher cognitive processes in the cortex. I will then present a relatively simple computational approach to modelling the ponto-cerebel lar auditory pathways and its application to the automatic classification of mouse calls. Finally I will outline the advantages of this approach to modelling animal vocal behaviour compared to current manual methods.\nSpea kers:\nAssociate Professor Neil McLachlan (Melbourne School of Psychologic al Sciences\, University of Melbourne) LOCATION:Le Gros Clark Building (Large Lecture Theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/fa1f4217-dc0f-4e37-9d6b-4f06ddebc139/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Mouse Talk: The applications of neurobiological models of mammalian hearing to the classification of mouse vocalizations - Associat e Professor Neil McLachlan (Melbourne School of Psychological Sciences\, U niversity of Melbourne) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Impact of inflammation on the perinatal brain - Pierre Gressens MD PhD (Inserm U1141 and Université Paris Diderot\, Paris & Centre for the Developing Brain\, KCL\, London) DTSTART;VALUE=DATE-TIME:20151218T120000Z DTEND;VALUE=DATE-TIME:20151218T130000Z UID:https://talks.ox.ac.uk/talks/id/2841bb38-b975-40fe-9d4b-a056bfa63ad7/ DESCRIPTION:Epidemiological studies have shown a strong association betwee n perinatal infection / inflammation and brain damage in the newborn and/o r neurological handicap in survivors. Experimental studies have allowed to show a causal effect of infection / inflammation on perinatal brain damag e. \nInfection / inflammatory factors can induce brain damage by themselve s. Accordingly\, injection of E Coli to pregnant rabbits induces periventr icular white matter cysts and widespread white matter cell death\, mimicki ng brain damage observed in preterm infants. In addition\, injection of Ur eaplasma Parvum to pregnant mice induces myelin defects and loss of intern eurons in the offspring. Similarly\, injection of LPS to pregnant rats ind uces transient central inflammation and myelination defects in the offspri ng. \nAlternatively\, in the so-called multiple hit hypothesis\, infection / inflammation can act as predisposing factors making the brain more susc eptible to a second stress (sensitization process). Indeed\, injection of low doses LPS to developing rats makes the newborn brain significantly mor e susceptible to hypoxic-ischemic insult. Similarly\, injection of interle ukin-1-beta to newborn mice or rats makes the brain much more sensitive to an excitotoxic insult. Current studies are evaluating the time window dur ing which sensitization of the brain will persist after exposure to inflam matory factors in the perinatal period. In addition\, the mechanisms by wh ich sensitization is working are not yet fully undertsood but could includ e changes in gene transcription and modifications of glutamate receptor ac tivity. \nEpidemiological data also suggest that perinatal exposure to inf lammatory factors could predispose to long term diseases including psychia tric disorders. This could be particularly the case for preterm infants wh ose brain could be more sensitive to environmental factors when compared t o full term infants. In this context\, exposure of newborn mice to low dos es of interleukin-1-beta during the neonatal period has been recently show n to disrupt oligodendrocyte maturation\, myelin formation and axonal deve lopment. These white matetr abnormalities are moderate during the developm ental period but do persist until adulthood. They lead to permanent defici encies in behavioral tests without detectable effects on motor functions. The underlying molecular mechanisms include alterations of the transcripti on of genes implicated in oligodendrogenesis\, myelin formation and axonal maturation. \nAltogether\, these clinical and experimental data strongly support the hypothesis that exposure to infection / inflammation during pr egnancy or the eprinatal period is deleterious for the brain. This can lea d to the appearance of perinatal brain damage that can lead to long term n eurological and cognitive disabilities. In addition\, some data also sugge st that the perinatal exposure to inflammatory factors can alter the progr ams of brain development.\nSpeakers:\nPierre Gressens MD PhD (Inserm U1141 and Université Paris Diderot\, Paris & Centre for the Developing Brain\, KCL\, London) LOCATION:Le Gros Clark Building (Large Lecture Theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/2841bb38-b975-40fe-9d4b-a056bfa63ad7/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Impact of inflammation on the perinatal brain - Pierre Gr essens MD PhD (Inserm U1141 and Université Paris Diderot\, Paris & Centre for the Developing Brain\, KCL\, London) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Maximising clinical relevance in small animal models of perinatal brain injury for mechanistic and neurotherapeutic trials - Bobbi Fleiss Ph D (Centre for the Developing Brain\, Perinatal Imaging & Health Imaging Sc iences & Biomedical\, Engineering Division\, King’s College London) DTSTART;VALUE=DATE-TIME:20151218T110000Z DTEND;VALUE=DATE-TIME:20151218T120000Z UID:https://talks.ox.ac.uk/talks/id/27ac7626-2b2f-46f1-872b-0a64b3438b30/ DESCRIPTION:Animal models of perinatal injury are the chief tools we have for understanding and developing therapies against perinatal brain injury. This is critical as perinatal brain injury causes immeasurable anguish fo r families and substantial on going costs for care and support of effected children. Interpretation of research data within the context of clinical observations and outcomes measures is paramount. This is due to the devel opmental and genetic differences between humans and research species. Furt hermore\, these differences also mean that no single model is capable of p roviding concrete certainly for predicting events in patient’s despite t here enormous utility. Thus\, within this presentation I will highlight th e key characteristics of multiple small animal models for mechanistic and neurotherapeutic trials\, and highlight examples of novel small animal phy siological and behavioural testing that gives small animal preclinical mod els greater clinical relevance.\nSpeakers:\nBobbi Fleiss PhD (Centre for t he Developing Brain\, Perinatal Imaging & Health Imaging Sciences & Biomed ical\, Engineering Division\, King’s College London) LOCATION:Le Gros Clark Building (Large Lecture Theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/27ac7626-2b2f-46f1-872b-0a64b3438b30/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Maximising clinical relevance in small animal models of p erinatal brain injury for mechanistic and neurotherapeutic trials - Bobbi Fleiss PhD (Centre for the Developing Brain\, Perinatal Imaging & Health I maging Sciences & Biomedical\, Engineering Division\, King’s College Lon don) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Novel behavioural phenotypes in the Neuroligin-3 genetic mouse mod el of Autism Spectrum Disorder - Emma Burrows PhD (Florey Institute of Neu roscience and Mental Health\, The University of Melbourne ) DTSTART;VALUE=DATE-TIME:20151016T160000 DTEND;VALUE=DATE-TIME:20151016T170000 UID:https://talks.ox.ac.uk/talks/id/09f8d38a-65de-495f-95ae-2f8fe9d9da4d/ DESCRIPTION:Rodent models are used to investigate mechanisms underlying be havioural traits in complex diseases such as Autism Spectrum Disorder (ASD ). To address the shortcomings of traditional rodent behavioural testing\, we are using touchscreens to test multiple cognitive domains in mice\, an alogous to those used in clinic assessments. Furthermore\, we are investig ating ultrasonic social calls as a proxy for communication impairments usi ng a novel sound recognition algorithm that was originally developed to de tect changes in affective prosody in humans with ASD. We are applying thes e novel methods to expand the behavioural characterisation of mice express ing the ASD-associated R451C mutation in the synaptic adhesion gene neurol igin-3 (NL3). Using touchscreens we have identified impaired behavioural f lexibility and subtle changes in attentional processing in the NL3 mouse. Our novel sound recognition algorithm is able to accurately characterise m ouse calls automatically and objectively\, and has uncovered impairments i n vocalisation in NL3 mice. Together\, these approaches have identified no vel behavioural phenotypes\, analogous to human ASD behaviours.\nSpeakers: \nEmma Burrows PhD (Florey Institute of Neuroscience and Mental Health\, T he University of Melbourne ) LOCATION:Le Gros Clark Building (Large Lecture Theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/09f8d38a-65de-495f-95ae-2f8fe9d9da4d/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Novel behavioural phenotypes in the Neuroligin-3 genetic mouse model of Autism Spectrum Disorder - Emma Burrows PhD (Florey Institu te of Neuroscience and Mental Health\, The University of Melbourne ) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Astrocyte roles in CNS injury and disease - Prof Michael Sofroniew \, MD PhD (Department of Neurobiology\, David Geffen School of Medicine\, UCLA\, USA) DTSTART;VALUE=DATE-TIME:20151029T160000Z DTEND;VALUE=DATE-TIME:20151029T170000Z UID:https://talks.ox.ac.uk/talks/id/91a5a759-34d8-4d8e-80fd-978e071668df/ DESCRIPTION:\nSpeakers:\nProf Michael Sofroniew\, MD PhD (Department of Ne urobiology\, David Geffen School of Medicine\, UCLA\, USA) LOCATION:Le Gros Clark Building (Large Lecture Theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/91a5a759-34d8-4d8e-80fd-978e071668df/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Astrocyte roles in CNS injury and disease - Prof Michael Sofroniew\, MD PhD (Department of Neurobiology\, David Geffen School of Me dicine\, UCLA\, USA) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Understanding how alterations in cortical circuitry modify behavio ral outputs - Prof Angelique Bordey\, PhD\, Professor of Neurosurgery and of Cellular and Molecular Physiology (Neurosurgery\, Yale School of Medici ne\, USA) DTSTART;VALUE=DATE-TIME:20150910T160000 DTEND;VALUE=DATE-TIME:20150910T170000 UID:https://talks.ox.ac.uk/talks/id/bc891bf5-7673-43c5-abbc-613b3d1c48a6/ DESCRIPTION:My lab aims at understanding the cellular and molecular underp innings of neuropsychiatric symptoms and epilepsy resulting from alteratio ns in cortical development. We have focused on a neurodevelopmental disord er Tuberous Sclerosis Complex (TSC). TSC is an autosomal dominant multisys tem disorder occurring in 1/6\,000 individuals with mutations in TSC1 or T SC2 leading to malformation of cortical development associated with seizur es and worsening of cognitive and psychiatric deficits. The ultimate goal is to find treatments for preventing or rescuing the anatomical defects an d associated symptoms.\nMost of our work is performed in vivo using a comb ination of sophisticated tools including in utero electroporation combined with EEG recordings in adult mice\, patch clamp electrophysiology\, trans lating ribosome affinity purification followed by microarray\, behavioral assessment\, and the use of conditional system based on tamoxifen injectio ns. Through these precise approaches\, we have recently generated a novel murine model of focal cortical malformations that are associated with soci al deficits and can be generated with or without daily convulsive seizures . This model opens the door for uncovering the anatomical\, biochemical\, and electrophysiological defects associated with behavioral symptoms.\nSpe akers:\nProf Angelique Bordey\, PhD\, Professor of Neurosurgery and of Cel lular and Molecular Physiology (Neurosurgery\, Yale School of Medicine\, U SA) LOCATION:Le Gros Clark Building (Large Lecture Theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/bc891bf5-7673-43c5-abbc-613b3d1c48a6/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Understanding how alterations in cortical circuitry modif y behavioral outputs - Prof Angelique Bordey\, PhD\, Professor of Neurosur gery and of Cellular and Molecular Physiology (Neurosurgery\, Yale School of Medicine\, USA) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:The role of the subplate layer in radial neuronal migration and co rtical - Chiaki Ohtaka-Maruyama\, PhD (Department of Brain Development and Neural Regeneration\, Tokyo Metropolitan Institute of Medical Science\, J apan) DTSTART;VALUE=DATE-TIME:20150918T160000 DTEND;VALUE=DATE-TIME:20150918T170000 UID:https://talks.ox.ac.uk/talks/id/9a5fc30a-fe64-4265-be91-15c922d3be91/ DESCRIPTION:During the formation of mammalian six-layered neocortical stru cture\, newborn neurons depart the ventricular zone and migrate toward the pial surface. At a middle stage of cortical development\, newly different iated postmitotic neurons show multipolar shape (MP)\, and move non-radial ly in the intermediate zone (multipolar migration). When these multipolar neurons pass through the subplate (SP) layer\, they show dynamic morpholog ical changes and adopt bipolar shape (BP). Then\, they migrate toward the pial surface (locomotion). Many KO mice with radial migration defects show abnormal MP-BP conversion at the SP suggesting that the interaction betwe en migrating neurons and SP layer plays critical roles in switching the mi gration mode. SP neurons are known to help thalamocortical innervation du ring early stage of neural circuit formation\, but their roles in radial n euronal migration remain to be elucidated. Our present working hypothesis is that MP neurons receive certain signals from the SP to change their mor phology and migration mode. To test our hypothesis\, we are analyzing the interaction between migrating young neurons and SP in many aspects. In thi s context\, we examined neuronal activity of SP neurons by Ca2+-imaging us ing GCaMP3\, and observed that they exhibited calcium oscillations at E15. Moreover\, we found that suppression of neuronal activities of SP neurons by electroporation of inward-rectifier potassium ion channel Kir2.1 led t o the impairment of radial migration. This suggests that neuronal activity of SP neurons is critical for radial migration. I will also discuss the e volutionally aspect of this study. \nSpeakers:\nChiaki Ohtaka-Maruyama\, P hD (Department of Brain Development and Neural Regeneration\, Tokyo Metrop olitan Institute of Medical Science\, Japan) LOCATION:Le Gros Clark Building (Large Lecture Theatre)\, off South Parks Road OX1 3QX TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/9a5fc30a-fe64-4265-be91-15c922d3be91/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:The role of the subplate layer in radial neuronal migrati on and cortical - Chiaki Ohtaka-Maruyama\, PhD (Department of Brain Develo pment and Neural Regeneration\, Tokyo Metropolitan Institute of Medical Sc ience\, Japan) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Recent insights into remote fear memory attenuation DTSTART;VALUE=DATE-TIME:20160310T160000Z DTEND;VALUE=DATE-TIME:20160310T173000Z UID:https://talks.ox.ac.uk/talks/id/7ff4f901-2aa9-4ab4-b26d-3dd452e8a0ce/ DESCRIPTION: LOCATION:Sherrington Building (The Sherrington Library\, Sherrington Build ing\, DPAG )\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/7ff4f901-2aa9-4ab4-b26d-3dd452e8a0ce/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Recent insights into remote fear memory attenuation TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Thalamocortical Interactions - Professor Andrew King (University o f Oxford)\, Professor Zoltan Molnar (University of Oxford )\, Dr Tim Vogel s\, Dr Holly Bridge (University of Oxford )\, Professor Simon Butt (Univer sity of Oxford )\, Miss Jacqui Stacey (University of Oxford )\, Dr Anna Ho erder Suabedissen (University of Oxford)\, Dr Louise Upton (University of Oxford)\, Mr Michael Lohse (University of Oxford)\, Mr Sebastian Vásquez- López\, Dr Tommas Ellender (University of Oxford) DTSTART;VALUE=DATE-TIME:20160504T140000 DTEND;VALUE=DATE-TIME:20160504T173000 UID:https://talks.ox.ac.uk/talks/id/dd26fe1d-db11-44dd-b760-977aef2e1cb8/ DESCRIPTION:2:00 PM – Introduction (Zoltán Molnár and Andy King)\n2:05 “Introduction” Prof Ray Guillery\, MRC Brain Network Dynamics Unit\, Oxford\n2:10 – "A View of Cortex from the Thalamus” Prof Murray Sherma n Department of Neurobiology\, The University of Chicago\, Chicago\, USA\n 3:15 – Tea/Coffee\n3:45 – "Thalamocortical Interactions in Cognition: what's the mediodorsal thalamus doing?” Anna S Mitchell\, Wellcome Tru st Senior Research Fellow\, Department of Experimental Psychology\, Univer sity of Oxford \n4:15 - Mini Presentations with focus on transthalamic cor tical communications \n(3 slides and 5 minutes max + 5 minutes questions)\ n4:15 - Holly Bridge “Cross modal plasticity in the thalamus”\n4:25 - Tim Vogels “Conceptual models of cortical function and development”\n4 :35 - Simon Butt and Jacqui Stacey “Does subplate have any role to play in thalamocortical development in somatosensory cortex?”\n4:45 - Anna Ho erder Suabedissen\, Louise Upton and Zoltán Molnár “Subplate/cortical layer 6b targets higher order thalamic nuclei”. \n4:55 - Michael Lohse ”The role of corticothalamic modulation in auditory perception.”\n5:05 - Sebastian Vásquez-López “Functional distribution of thalamocortical inputs to the mouse auditory cortex: a dual-colour calcium imaging study. ” \n5:15 – Tommas Ellender “Corticostriatal interactions.”\n5:25 - GENERAL DISCUSSION WITH REFRESHMENTS\n\nSpeakers:\nProfessor Andrew King (University of Oxford)\, Professor Zoltan Molnar (University of Oxford )\, Dr Tim Vogels\, Dr Holly Bridge (University of Oxford )\, Professor Simon Butt (University of Oxford )\, Miss Jacqui Stacey (University of Oxford ) \, Dr Anna Hoerder Suabedissen (University of Oxford)\, Dr Louise Upton (U niversity of Oxford)\, Mr Michael Lohse (University of Oxford)\, Mr Sebast ian Vásquez-López\, Dr Tommas Ellender (University of Oxford) LOCATION:Sherrington Building (Sherrington Library\, DPAG)\, off Parks Roa d OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/dd26fe1d-db11-44dd-b760-977aef2e1cb8/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Thalamocortical Interactions - Professor Andrew King (Uni versity of Oxford)\, Professor Zoltan Molnar (University of Oxford )\, Dr Tim Vogels\, Dr Holly Bridge (University of Oxford )\, Professor Simon But t (University of Oxford )\, Miss Jacqui Stacey (University of Oxford )\, D r Anna Hoerder Suabedissen (University of Oxford)\, Dr Louise Upton (Unive rsity of Oxford)\, Mr Michael Lohse (University of Oxford)\, Mr Sebastian Vásquez-López\, Dr Tommas Ellender (University of Oxford) TRIGGER:-PT1H END:VALARM END:VEVENT BEGIN:VEVENT SUMMARY:Neural Dynamics in Prefrontal Cortex: Ensemble Codes\, Oscillatory Structure and Avalanches during short-term memory - Dr Matthias Munk (Uni versity of Tübingen and Systems Neurophysiology\, Technical University Da rmstadt) DTSTART;VALUE=DATE-TIME:20160613T150000 DTEND;VALUE=DATE-TIME:20160613T160000 UID:https://talks.ox.ac.uk/talks/id/e91be5e8-c020-45b6-9bb5-6fea9b08239d/ DESCRIPTION:The concepts for neuronal coding during short-term or working memory have recently been challenged by observations that do no longer sup port an exclusive role of sustained firing in maintaining information. We have studied alternative neural signals like LFP oscillations and higher o rder spike synchronization which reveal interesting options for engaging c ortical circuitry in the maintenance of information about stimuli in short -term memory. I will discuss our findings in the light of multiple oscilla tory rhythms and measures of global system dynamics which may serve as coo rdinating principles of memory processes.\nSpeakers:\nDr Matthias Munk (Un iversity of Tübingen and Systems Neurophysiology\, Technical University D armstadt) LOCATION:Sherrington Building (Sherrington Room\, Sherrington Building\, D PAG)\, off Parks Road OX1 3PT TZID:Europe/London URL:https://talks.ox.ac.uk/talks/id/e91be5e8-c020-45b6-9bb5-6fea9b08239d/ BEGIN:VALARM ACTION:display DESCRIPTION:Talk:Neural Dynamics in Prefrontal Cortex: Ensemble Codes\, Os cillatory Structure and Avalanches during short-term memory - Dr Matthias Munk (University of Tübingen and Systems Neurophysiology\, Technical Univ ersity Darmstadt) TRIGGER:-PT1H END:VALARM END:VEVENT END:VCALENDAR